Double-stranded DNA (dsDNA) serves as a fundamental repository of genetic information and plays a pivotal role in the diagnosis and therapeutic management of diseases. However, the inherent stability of the DNA double helix under physiological conditions presents a challenge in accessing internal bases. To address this, various molecular targeting technologies have been developed, offering high specificity while destabilizing the DNA structure. This review provides a comprehensive overview of current dsDNA targeting tools, such as hybridization probes, modified nucleic acid probes, zinc finger proteins (ZFPs), transcription activator-like effector nucleases (TALENs), the CRISPR/Cas system, Argonaute proteins (Agos), and the lambda exonuclease-pDNA system (λ Exo-pDNA), and some cutting-edge molecular tools. It delves into the mechanisms behind these technologies. It highlights their applications in diverse areas, including in vitro detection, in situ imaging, gene editing, and their integration with artificial intelligence (AI)-driven tools. Additionally, the review compares these techniques, discusses future technological opportunities, and identifies challenges in integrating these tools into diagnostic and therapeutic practices. By providing a holistic view of these rapidly evolving technologies, this review aims to fill a gap in the current literature and explore the future potential of dsDNA targeting innovations.

The intricate interplay between polyaniline (PANI) and waterborne polyurethane (WPU) matrices during saline aging remains elusive, particularly regarding the dynamic reorganization of hydrogen bond networks and microphase separation structures. Herein, we report a systematic investigation into the "structure-property" evolution pathway of PANI/WPU composites through three distinct stages: pristine, saline-swollen, and redried states. Phytic acid (PA)-doped PANI (PANI-PA) was synthesized via in-situ oxidative polymerization and incorporated into WPU to fabricate composite coatings. FTIR and DMA analyses reveal that PANI introduction competitively disrupts intra-/inter-chain hydrogen bonding within WPU hard segments, resulting in decreased apparent crosslink density yet elevated glass transition temperature in the pristine state. Upon saline swelling, PANI synergizes with water molecules to facilitate more complete dissociation of urea domains compared to pristine WPU. Notably, during redrying, PANI surfaces serve as heterogeneous nucleation sites, guiding the ordered reassembly of hard segments and enabling "synergistic recovery" of the hydrogen bond network-whereas neat WPU suffers irreversible network damage. Laser confocal microscopy confirms that this PANI-induced structural reorganization leads to a dramatic similar to 7.2-fold increase in surface roughness post-redrying. Electrochemical impedance spectroscopy demonstrates that WPU/PANI coatings maintain low-frequency impedance modulus (|Z|(0.01Hz)) at 10(8) Omega & centerdot;cm(2) magnitude after 28-day immersion, exhibiting active protection capability via passivation film formation on the steel substrate. Due to the absence of an ideal rubbery plateau in DMA tests, apparent crosslink densities reported herein are strictly comparative across samples and states. These findings elucidate that PANI regulates WPU matrix properties through a dual mechanism involving interfacial hydrogen bonding chemistry and rigid-template-induced structural ordering, providing theoretical guidance for designing high-performance WPU composites with enhanced aging resistance.

Engineered in vitro cardiac tissues are being developed and increasingly used for disease modeling and drug evaluation, but reproducing cardiac cell composition and three-dimensional architecture alone does not ensure physiologically meaningful function. Native myocardial performance arises from coordinated electrical activation, active force generation, and passive mechanical resistance governed by stiffness, anisotropy, nonlinear elasticity, and viscoelastic relaxation. Failure to reproduce these coupled properties can alter force transmission, tissue deformation, mechanosensitive cellular responses, and the interpretation of disease phenotypes or drug effects. Yet myocardial mechanics, computational modeling, biomaterial design, and biofabrication are commonly developed as separate domains. This review integrates these areas through a biomechanics-guided property-parameter-function framework. We first examine the multiscale structural determinants of myocardial mechanics and critically compare cellular, continuum, phenomenological, microstructure-informed, viscoelastic, and pathology-informed models with respect to predictive scope, computational demand, parameter identifiability, experimental validation, and engineering relevance. We then show how model-derived descriptors-including active stress, baseline and nonlinear stiffness, anisotropy, relaxation behavior, and remodeling-related parameters-can be translated into controllable biomaterial properties, scaffold architecture, fabrication and conditioning protocols, and mechanical boundary conditions. Emerging approaches involving artificial intelligence, inverse design, uncertainty quantification, and digital twins are discussed as routes toward adaptive and patient-relevant tissue models. By positioning computational biomechanics as a design and validation tool, this review provides a systematic basis for engineering cardiac tissues with more predictable mechanical function and more reproducible disease- and drug-response readouts.

BACKGROUND:Viruses continue to threaten global health, highlighting the urgent need for antiviral strategies with broad-spectrum activity. The nucleocapsid (N) protein undergoes liquid-liquid phase separation (LLPS), a conserved process essential for viral assembly. However, pharmacological targeting of this process remains largely unexplored. PURPOSE:This study aimed to establish a high-content screening platform to discover small-molecule inhibitors of the conserved LLPS of the SARS-CoV-2 nucleocapsid protein and to evaluate their broad-spectrum antiviral activity and anti-inflammatory effects. METHODS:We established a high-content imaging-based screening platform to identify small-molecule inhibitors of SARS-CoV-2 nucleocapsid protein LLPS. Candidate compounds were evaluated for antiviral activity using immunofluorescence microscopy, quantitative RT-PCR, and virus-like particle systems. Antiviral efficacy and immunomodulatory effects were further validated in SARS-CoV-2-infected cell and mouse models. RESULTS:We identified tannic acid (TA) as a potent inhibitor that disrupts nucleocapsid protein condensation by binding to multiple regions of nucleocapsid and interfering with nucleocapsid-RNA interactions. Tannic acid robustly suppressed SARS-CoV-2 replication in vitro and in vivo. In parallel, tannic acid attenuated virus-induced inflammatory responses by interacting with G3BP1 and suppressing NF-κB signaling. Importantly, tannic acid maintained inhibitory activity against nucleocapsid proteins from major SARS-CoV-2 variants and exhibited broad-spectrum antiviral effects against multiple human coronaviruses, influenza A virus, and vesicular stomatitis virus. CONCLUSIONS:These findings demonstrate that targeting nucleocapsid protein LLPS represents a conserved antiviral strategy resilient to viral evolution and identify tannic acid as a promising lead compound with dual antiviral and anti-inflammatory properties.

Interferon (IFN) signalling is essential for antiviral defence yet pathogenic in autoimmunity, however, the mechanisms orchestrating this duality remain poorly defined. Here, we identify USP30-AS1, a cytoplasmic long non-coding RNA (lncRNA) induced by type I IFN, as a pivotal post-transcriptional amplifier of innate immunity. We demonstrate that USP30-AS1 selectively enhances the mRNA stability of nucleic acid sensors. Moreover, USP30-AS1 preferentially stabilizes the majority of AU-rich element (ARE)-containing interferon-stimulated gene (ISG) mRNAs. USP30-AS1 executes this function independently of its antisense partner, USP30. The deletion of USP30-AS1 impaired IFN-β-mediated antiviral defence and suppressed pro-inflammatory cytokine production. Consistent with its role in amplifying immune responses, USP30-AS1 was markedly upregulated in human autoimmune diseases characterised by dysregulated IFN signalling, including systemic lupus erythematosus, rheumatoid arthritis, and dermatomyositis. Thus, our work unveils USP30-AS1 as a key regulator that fine-tunes the stability of nucleic acid sensors and ARE-containing immune transcripts, providing a direct mechanistic link between IFN signalling and post-transcriptional gene regulation. These findings establish USP30-AS1 as a critical rheostat for immune homeostasis and a promising therapeutic target for IFN-associated diseases.

African swine fever virus (ASFV) is a lethal pathogen that triggers uncontrolled cytokine storms and severe immunopathology. However, the viral factors responsible for systemic inflammation remain unclear. Here, we show that the ASFV-encoded proteins MGF_110-3L and MGF_110-4L are secreted via the conventional ER-Golgi pathway. Single-cell RNA sequencing of porcine PBMCs revealed that MGF_110-3L preferentially activates inflammatory responses in monocytic cells. Mechanistically, both proteins bind Toll-like receptor 2 (TLR2) and signal through TLR2/TLR1 and TLR2/TLR6 heterocomplexes, with the co-receptor CD14 enhancing ligand recognition and signal amplification. These interactions activate MyD88-dependent NF-κB signaling, leading to robust induction of proinflammatory cytokines. ASFV strains lacking either MGF_110-3L or MGF_110-4L cause attenuated cytokine responses in vitro and impaired inflammatory pathology in pigs. Together, these findings establish MGF_110-3L and MGF_110-4L as secreted virulence factors that subvert innate immune recognition and drive lethal inflammation, highlighting their potential as targets for antiviral and vaccine development.

The development of high-performance polymeric coatings with superior mechanical properties and excellent corrosion resistance remains a critical challenge for materials used in harsh marine environments. This study presents an integrated design strategy combining tailoring the molecular structure of the polymer, promoting strong interfacial interactions between the coating and the substrate, and the construction of a multidimensional barrier to achieve synergistic optimization of a coating with a stiffness-toughness balance and excellent longterm anti-corrosion performance. Composites of a polyurethane and graphene nanoplatelets (PU/GNP) were prepared via in-situ polymerization using poly(tetramethylene ether glycol) (PTMEG) and poly(dimethylsiloxane) (PDMS) as PU soft segments, hexamethylene diisocyanate (HMDI) as a hydrolysis-resistant hard segment, and a binary chain extender system consisting of 1,4-butanediol (BDO) and 3,3 '-dichloro-4,4 '-diaminodiphenylmethane (MOCA). Fourier transform infrared (FTIR) spectroscopy and X-ray photoelectron (XPS) spectroscopy confirmed strong interfacial interactions between GNP and the PU matrix, with the hydrogenbonding index reaching a maximum of 9.65 for a 0.1 wt% GNP loading. Microstructural characterization identified 0.1 wt% as the optimal filler concentration for uniform GNP dispersion in the PU matrix. This composite (PUg-0.1) displayed outstanding overall performance: a tensile strength of 14.58 MPa (345% higher than pure PU) and an elongation at break of 427% (65% higher), overcoming the traditional strength-toughness trade-off required for such coatings. An apparent crosslinking density of 6.4 & times; 10- 2 mol/cm3 was determined from dynamic mechanical analysis, twice that of pure PU. Electrochemical impedance spectroscopy (EIS) revealed an ultra-high protection level with a low-frequency impedance modulus |Z|0.01Hz, of 1.71 & times; 1011 Omega & sdot;cm2 (an enhancement of 5 orders of magnitude compared to unfilled PU), and water absorption below 0.9 wt% in deionized water (1.45 wt% in saline). Salt spray testing confirmed excellent coating surface integrity over 48 days of exposure, accompanied by self-limiting and damage-tolerant corrosion behavior. A "surface-interface-bulk" triple synergistic mechanism is proposed which provides a theoretical basis for the design of long-life anti-corrosion protective coatings for application in aggressive environments.

A synergistic two-step strategy integrating molecular end-capping with biomass filler reinforcement was developed to overcome the inherent trade-offs among mechanical strength, water resistance, and corrosion protection in polyurethane (PU) coatings. Maleimide end-capping agents with different structures were systematically screened, and 4-hydroxyphenylmaleimide (4-HPM) was identified as optimal, yielding the highest hydrogen-bonding index (HBI = 4.11) and balanced mechanical properties (tensile strength of 14.70 MPa and elongation at break of 1412%). Alkaline lignin (AL), an industrial by-product from pulping processes, was then introduced as a renewable hydrogen-bond reinforcing filler into the 4-HPM-capped PU matrix. At an optimal loading of 1wt.‰, AL achieved uniform dispersion and provided supplementary hydrogen-bonding sites, increasing crosslinking density and hard-segment order. The resulting composite (PUM-1) exhibited a tensile strength of 30.44 MPa, an elongation at break of 1232%, a water contact angle of 84.7°, and a low-frequency impedance modulus of 1.94 × 1010 Ω·cm2, with long-term stability in salt spray tests. Excessive AL loading (≥5wt.‰) caused aggregation and hydrophilic defects, disrupting the network. Notably, maximization of structural parameters (HBI = 5.55) did not translate to optimal corrosion protection; balanced dispersion and crosslinking uniformity governed long-term performance. This work establishes quantitative design rules for biomass-reinforced high-performance anticorrosion coatings.

Brucellosis is a widespread zoonotic disease caused by Brucella, a genus of facultative intracellular bacteria that infects livestock and humans. Brucella primarily replicates within the endoplasmic reticulum (ER) of host cells, where it establishes a specialized replicative niche. This ER localization disrupts ER structure and induces ER stress. The unfolded protein response (UPR) is a critical cellular pathway that maintains ER homeostasis by restoring protein-folding capacity and regulating stress responses. However, how Brucella manipulates host UPR pathways to promote its intracellular survival and pathogenesis remains poorly understood. Here, we identify the Brucella outer membrane protein Omp25 as a key factor in promoting its intracellular survival and proliferation by activating the host UPR. Omp25 directly binds to the ER chaperone binding-immunoglobulin protein, inducing the release and activation of the UPR sensors, PKR-like ER kinase, inositol-requiring enzyme 1 alpha, and activating transcription factor 6, thereby modulating ER homeostasis to favor bacterial replication. In addition, Omp25 enhances inflammatory cytokine expression via the binding-immunoglobulin protein-inositol-requiring enzyme 1 alpha-NF-κB signaling axis. The omp25-deleted strains (Δomp25) show impaired intracellular replication and reduced UPR activation and result in attenuated induction of inflammatory genes in infected cells compared with WT strains. In vivo, mice infected with an omp25 mutant strain exhibit lower bacterial burdens and milder tissue pathology compared with mice infected with the WT strain. These findings uncover a mechanism by which Omp25 facilitates Brucella intracellular proliferation through UPR modulation and highlight Omp25 as a potential target for therapeutic interventions and next-generation attenuated vaccines.

The development of high-performance carbon materials for electrochemical energy storage has relied on precise control over atomic configurations. However, conventional nitrogen-doping methods typically produced random dopant distributions and mixed configurations, which limited the improvement of electrochemical activity. In this work, we demonstrated that structural defects intrinsically directed the selective incorporation of highly active nitrogen atoms at edge sites of the carbon skeleton, achieving defect-induced precise edge-N (N-5 and N-6) doping. High-power ultrasonication introduced numerous structural defects, mainly new zigzag edges, into the two-dimensional graphene lattice. Multi-scale analyses, from bulk spectroscopies (XPS, EPR) to atomic-resolution EELS mapping, demonstrated that N atoms were concentrated at edge regions, predominantly forming edge-N configurations with the pi*/sigma* ratio nearly 10 times higher than that of the in-plane region. By analyzing the N doping process (up to 600 degrees C), it was found that the healing of carbon structure defects was limited within this temperature range. These defect sites exhibited stronger adsorption toward NH3 than the basal plane proved by density functional theory (DFT) calculations as the energetic basis, and NH3 indeed preferentially attacked defect sites passivated by H or O-containing groups. Consequently, the abundant and persistent defects under 600 degrees C as active sites led to a gradual increase in total nitrogen content while maintaining a high and stable proportion of edge-N (similar to 72%). When the temperature exceeded 600 degrees C, both the overall nitrogen content and the proportion of edge-N decreased. The defect-engineered graphene (sN-C-600) exhibited a 116.8% increase in specific capacitance relative to its undoped counterpart and delivered a 24.9% higher capacitance than the non-defect sample (LN-C-600). Overall, this study established structural defects as active regulators of N heteroatom incorporation, providing design guidance for constructing carbon electrodes with controllable edge chemistry and optimized electrochemical functionality.

African swine fever virus (ASFV) infection induces cellular stress that activates the unfolded protein response (UPR), a key pathway for restoring endoplasmic reticulum (ER) homeostasis. However, the mechanisms by which ASFV modulates the UPR remain incompletely understood. Here, we identify the ASFV protein MGF_110-8L as a key regulator of the UPR, leading to the dissociation and activation of the UPR sensors PERK, IRE1α, and ATF6, which subsequently restore ER homeostasis. Moreover, MGF_110-8L triggers UPR-dependent autophagy, which in turn contributes to the suppression of type I interferon-mediated immune responses. Deletion of MGF_110-8L (ASFV-Δ8 L) markedly reduced the activation of both UPR and autophagy pathways and led to enhanced type I interferon responses. Together, our findings reveal a novel mechanism by which an ASFV protein activates the host UPR-autophagy axis to restore cellular homeostasis and modulate host innate immunity, highlighting MGF_110-8L as a potential target for therapeutic development.

High-strength electrochemical corrosion-resistant materials hold significant application value in marine engineering and construction sectors. In this study, cellulose nanocrystals (CNCs) extracted from microcrystalline cellulose (MCC) via sulfuric acid hydrolysis were incorporated into polyurethane (PU) through in situ polymerization to systematically investigate the effects of CNC addition timing (soft segment, hard segment, chain extender, and prepolymer stages) on material properties. Low-field nuclear magnetic resonance (LF-NMR) relaxation analysis revealed that introducing CNC during the prepolymer stage most dramatically enhanced molecular chain rigidity, as evidenced by the most pronounced relaxation decay. Fourier transform infrared spectroscopy (FTIR) confirmed that CNC incorporation significantly increased the hydrogen bonding index (HBI), with later addition stages yielding greater HBI enhancement. Dynamic mechanical analysis (DMA) further demonstrated that prepolymer-stage CNC addition substantially improved dynamic cross-linking density, thereby endowing the composites with superior mechanical performance. Electrochemical impedance spectroscopy (EIS) measurements showed a remarkable 2-4 orders of magnitude increase in impedance modulus for all PU/CNC composites, validating CNC's corrosion protection efficacy.

The microenvironment has been recognized as a critical determinant in the pathogenesis of cancer, autoimmune diseases, and allergy. Effective therapies must therefore target the microenvironment to achieve either immune activation or immune tolerance, depending on the disease context. Recent advances in nanocomposite-based therapeutics have provided new opportunities to precisely modulate immune microenvironments and improve therapeutic efficacy. This short review summarizes recent progress and ongoing challenges in this rapidly evolving field. We discuss how targeted immune modulation has revolutionized modern medicine by selectively adjusting immune responses, enhancing immunity against cancers and infectious diseases, or inducing tolerance in autoimmune and allergic disorders. Finally, we highlight how nanotechnology-driven microenvironment targeting enhances specificity, minimizes off-target effects, and offers a powerful platform for next-generation immune therapies.

Plastic-Metal hybrids have gained significant attention in automotive and aerospace fields. In the study, the silane was introduced on the surface of anodized micro-nano porous aluminum alloy (Al) plate. The silanized Al sample was then joined with polybutylene terephthalate (PBT) specimen by ultrasonic-assisted hot pressing technology to manufacture hybrid. The interfacial physical embedding structure plays an important role in plastic-metal joining and the scanning electron microscope (SEM) results demonstrated that effective mechanical interlocking was achieved between PBT and Al. X-ray Photoelectron Spectroscopy (XPS) results demonstrated the new chemical bonds occurred at the PBT-Al interface, which acted as bridges in the PBT-Al interface joining. Due to synergistic effect of physical embedding and chemical bonding, the maximum adhesion strength reached 36.3 MPa when the silane concentration was 4 %, which was 37 % higher than that without silane treatment. When the silane concentration exceeds 4 %, leading to blocking pores on the anodized aluminum alloy surface, resulting in a decrease in adhesion strength. In conclusion, these results can provide some ideas and help for the development of subsequent plastic-metal hybrids and practical applications.

Pulmonary fibrosis (PF) is a chronic and progressive interstitial lung disease characterized by abnormal scarring of lung tissue, which severely impairs respiratory function and diminishes quality of life. Despite the availability of antifibrotic and immunosuppressive treatments, therapeutic outcomes remain limited. Inhalable nanomedicines represent a promising approach to address the limitations of traditional therapies by overcoming the lung’s complex physiological and pathological barriers, such as respiratory airflow dynamics, mucus absorption, macrophage clearance, surfactant interactions, and the influence of the lung microbiome. This review delves into the intricate interactions between inhalable nanoparticles and the lung environment, exploring recent advancements in nanotechnology that enable efficient and targeted drug delivery to the fibrotic lung. Key areas of focus include optimizing nanoparticle design, overcoming lung barriers, addressing the challenges of fibrotic pathology, and leveraging biomimetic and “smart” approaches for targeted therapies. This work aims to provide insights into the future of inhalable nanomedicines, paving the way for more effective, personalized treatments for pulmonary fibrosis with improved therapeutic outcomes and minimal side effects.

Bitumen without modification is prone to suffer from damage under extreme temperature and traffic conditions, leading to distress such as rutting, fatigue cracking, and thermal cracking. Polyurethane-modified bitumen can effectively be prepared at lower temperatures and combine low-carbon and environmental-protection concepts. The resulted polyurethane can also improve the in-service performance of bitumen, such as rutting resistance. In this study, a polyurethane prepolymer (PU) based on polypropylene glycol (PPG) and diphenylmethane diisocyanate (MDI) as the soft and hard segments and 3,3'-dichloro-4,4'-diaminodiphenylmethane (MOCA) as a chain extender was synthesized and used to modify the viscoelastic behavior of bitumen. The interaction between the PU prepolymer and unreacted MDI and the polar groups present on the base bitumen provides a route to enhancing the miscibility between the blend components. The rheological behavior of the bitumen, with varying PU content, was investigated from strain sweep and time sweep measurements, with particular attention given to the analysis of Lissajous-Bowditch (LB) curves and the normalized third relative intensities (I3/I1). Three different methods based on strain sweep tests were employed to determine the critical strain at which the viscoelastic behavior transitions from the linear to nonlinear regime. The distinct rheological behavior observed for bitumen with different PU content was supported from observations of the blend morphology and confirmation of interactions between blend components from Fourier transform infrared (FTIR) spectroscopy. This study reveals that the rheological behavior of a PU-modified bitumen is closely related to the combined effects of interfacial interaction, phase morphology, and phase distribution of the blend components. Illustrating this relationship can enable the design of tailored bituminous materials with excellent in-service performance.

Immunotherapy has become a prominent first-line cancer treatment strategy. In non-small cell lung cancer (NSCLC), the expression of PD-L1 induces an immuno-suppressive effect to protect cancer cells from immune elimination, which designates PD-L1 as an important target for immunotherapy. However, little is known about the regulation mechanism and the function of PD-L1 in lung cancer. In this study, we have discovered that KEAP1 serves as an E3 ligase to promote PD-L1 ubiquitination and degradation. We found that overexpression of KEAP1 suppressed tumor growth and promoted cytotoxic T-cell activation in vivo. These results indicate the important role of KEAP1 in anti-cancer immunity. Moreover, the combination of elevated KEAP1 expression with anti-PD-L1 immunotherapy resulted in a synergistic effect on both tumor growth and cytotoxic T-cell activation. Additionally, we found that the expressions of KEAP1 and PD-L1 were associated with NSCLC prognosis. In summary, our findings shed light on the mechanism of PD-L1 degradation and how NSCLC immune escape through KEAP1-PD-L1 signaling. Our results also suggest that KEAP1 agonist might be a potential clinical drug to boost anti-tumor immunity and improve immunotherapies in NSCLC.

The development of polymeric materials combining high mechanical strength with environmentally adaptive self-healing capability represents a key objective in smart materials research, particularly for wearable biomedical applications. This study synthesized a polyurethane-based material (PUAM) incorporating poly(N-isopropylacrylamide) (PNIPAM), and varying contents of custom-synthesized ureido-pyrimidinone (UPy) units with quadruple hydrogen bonds to investigate humidity-responsive self-healing behavior. Fourier transform infrared (FTIR) spectroscopy demonstrated a progressive increase in hydrogen bonding index (HBI) with higher UPy content. Dynamic mechanical analysis (DMA) further revealed monotonic enhancements in both storage modulus and dynamic crosslinking density (Vd). Optical microscopy observations of scratch closure under different humidity conditions and NaCl vapor environments confirmed effective humidity-responsive self-healing, with performance positively correlating with UPy concentration. Water contact angle and hygroscopicity measurements show that a high UPy content improves the moisture absorption performance of the material. The absorbed water molecules function as plasticizers to enhance polymer chain mobility and facilitate hydrogen bond reorganization, thereby improving self-healing performance. This work provides a feasible strategy for designing high-performance smart materials with tunable humidity-responsive healing properties.

Functional configurability is highly desired for flexible electronics to serve ever-changing and diverse application scenarios. In complementary metal-oxide-semiconductor (CMOS) logic circuits, functional configurations can be achieved at the most basic device level by modulating the P/N polarity of the field-effect transistors. The intrinsic ambipolarity of low-dimensional materials provides the possibility of configuring the polarity of the constructed transistors by selectively injecting carriers on demand with proper methodologies. In this study, we propose a strategy based on carbon nanotubes (CNTs), with the initial devices functioning as conventional p-type thin film transistors (TFTs), that achieves polarity configuration through reversible electrostatic doping by applying and removing a polymer doping layer on the channel area covered with a Y2O3 passivation layer. This method exhibits favorable characteristics, including high performance comparable to those of conventional devices under normal operation conditions, good P/N symmetry, large-scale uniformity, nonvolatile features, and robust stability. The resultant configurable TFTs facilitate the construction of a CMOS inverter with a rail-to-rail output and a high voltage gain exceeding 40. Basic circuit components such as diodes, rectifiers, and logic gates are constructed with reconfigurable functionalities. To illustrate its potential, we designed a reconfigurable CMOS circuit module that can be optionally programmed into four different functions─NAND, NOR, XOR, and XNOR, which can serve as a building block for constructing more complex reconfigurable integrated circuits, applicable in fields such as hardware security and adaptive monitoring.

Self-healing polyurethanes are garnering attention as a smart material, and has significant application potential in aerospace, biomedical, and electronics fields. In this paper, castor oil is selected as a soft segment in place of petroleum-based polyol to enhance the mechanical properties of polyurethane while improving the mobility of molecular chains. Meanwhile, a polyurethane with good self-healing properties was successfully prepared by selecting 2,2`-Diaminodiphenyl disulfide (DTDA) containing disulfide bonds as a chain extender. As the proportion of DTDA increases, the initial thermal decomposition temperature of polyurethane decreases by 21°C. Cutting and tensile tests confirmed the high mechanical properties and self-healing characteristics of the polyurethane network. And the self-healing efficiency of the polyurethane materials was improved by prolonging the healing time and increasing the healing temperature. As the content of disulfide bonds and hard segments increased, the tensile strength of polyurethane increases progressively, the elongation at break decreased, and the R(stress) and R(strain) of each specimen tended to increase and then decrease. The healing efficiency of the specimen with a disulfide bond content of 13.45