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Verified CAS / Academic Author2 Decoded Studies

Prof. HUANG Ben

Guilin Medical University, Guilin, 541000, China; People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530021, China; Guangxi University, Nanning, 530004, China

Research Publications & English Decoded Briefs

Showing 2 publications
SCIENCE CHINA Materials2026DOI: 10.1007/s40843-026-4249-2

Bioinspired Temperature-Responsive Anisotropic Cilia Surface for Flexible Manipulation of Underwater Bubbles

Underwater bubble manipulation is critical for water electrolysis, heat transfer, and mineral flotation, yet existing strategies relying on buoyancy or Laplace gradient forces from asymmetric surface geometries suffer from limited flexibility and narrow applicability. This work introduces a temperature-responsive anisotropic cilia surface (TRAS) that achieves bidirectional long-range bubble transport by modulating elastic modulus and stiffness. The TRAS enables precise control over the asymmetric three-phase contact line and viscous resistance, facilitating reversible bubble motion. Experimental validation using aqueous ethanol droplets with varying surface tensions (73.16 mN/m for 0 vol% to 22.27 mN/m for 100 vol%) on cilia with center-to-center spacings of 0.2–1.0 mm reveals that transport direction depends on both cilia spacing and liquid surface tension. Droplets of 0 vol% and 20 vol% ethanol exhibit sustained reverse transport on hard cilia, while 60 vol%, 80 vol%, and 100 vol% solutions show sustained forward transport. Notably, 40 vol% ethanol droplets display bidirectional transport at 0.6 mm spacing, reverse transport at 0.8 and 1.0 mm, and forward transport at 0.2 and 0.4 mm. These results demonstrate that tuning surface tension and cilia spacing provides a versatile platform for directional bubble manipulation, with promising applications in heat transfer, electrochemistry, and gas handling systems.

Environmental Chemistry2026DOI: 10.7524/j.issn.0254-6108.2026030601

Network Toxicology and Molecular Dynamics Simulation Elucidate Bisphenol A-Induced Neurotoxicity in SVGP12 Astrocytes: Mechanistic Insights and Risk Assessment for Chronic Neurodegenerative Diseases

Bisphenol A (BPA), a high-volume industrial chemical, is implicated in neurotoxicity and chronic neurodegenerative diseases. This study integrates network toxicology, molecular docking, and molecular dynamics simulations to systematically delineate the common mechanisms linking BPA to Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). Using the human astrocyte cell line SVGP12 as an in vitro model, we identified six key toxic functional proteins—TP53, HSP90AA1, HSP90AB1, INS, BCL2, and AKT1—that mediate BPA's effects across these diseases, with BCL2 emerging as the most central node. Experimental validation demonstrated that BPA induces oxidative stress and cell cycle arrest, suppresses the INS-AKT1-BCL2 anti-apoptotic pathway, and activates the TP53-HSP90 pro-apoptotic pathway, culminating in mitochondrial apoptosis of astrocytes and disruption of neural microenvironment homeostasis. These findings reveal a convergent mechanism by which BPA accelerates neurodegeneration, filling a critical gap in understanding BPA's role in AD, PD, and HD. The study provides a novel theoretical framework and experimental evidence for BPA neurotoxicity risk assessment and informs preventive and therapeutic strategies for BPA-related neurodegenerative disorders.