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Luciferase reporter systems are commonly used in scientific research to investigate a variety of biological processes, including antiviral innate immunity. These systems employ the use of luciferase enzymes derived from organisms such as fireflies or renilla reniformis, which emit light upon reaction with a substrate. In the context of antiviral innate immunity, the luciferase reporter systems offer a noninvasive and highly sensitive approach for real-time monitoring of immune responses in vitro and in vivo, enabling researchers to delve into the intricate interactions and signaling pathways involved in host-virus dynamic interactions. Here, we describe the methods of the promoter-luciferase reporter and enhancer-luciferase reporter, which provide insights into the transcriptional and post-transcriptional regulation of antiviral innate immunity. Additionally, we outline the split-luciferase complementary reporter method, which was designed to explore protein-protein interactions associated with antiviral immunity. These methodologies offer invaluable knowledge regarding the molecular mechanisms underlying antiviral immune pathways and have the potential to support the development of effective antiviral therapies.

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Spliceosome dysfunction and aberrant RNA splicing underline unresolved inflammation and immunopathogenesis. Here, we revealed the misregulation of mRNA splicing via the spliceosome in the pathogenesis of rheumatoid arthritis (RA). Among them, decreased expression of RNA binding motif protein 25 (RBM25) was identified as a major pathogenic factor in RA patients and experimental arthritis mice through increased proinflammatory mediator production and increased hyperinflammation in macrophages. Multiomics analyses of macrophages from RBM25-deficient mice revealed that the transcriptional enhancement of proinflammatory genes (including Il1b, Il6, and Cxcl10) was coupled with histone 3 lysine 9 acetylation (H3K9ac) and H3K27ac modifications as well as hypoxia inducible factor-1α (HIF-1α) activity. Furthermore, RBM25 directly bound to and mediated the 14th exon skipping of ATP citrate lyase (Acly) pre-mRNA, resulting in two distinct Acly isoforms, Acly Long (Acly L) and Acly Short (Acly S). In proinflammatory macrophages, Acly L was subjected to protein lactylation on lysine 918/995, whereas Acly S did not, which influenced its affinity for metabolic substrates and subsequent metabolic activity. RBM25 deficiency overwhelmingly increased the expression of the Acly S isoform, enhancing glycolysis and acetyl-CoA production for epigenetic remodeling, macrophage overactivation and tissue inflammatory injury. Finally, macrophage-specific deletion of RBM25 led to inflammaging, including spontaneous arthritis in various joints of mice and inflammation in multiple organs, which could be relieved by pharmacological inhibition of Acly. Overall, targeting the RBM25-Acly splicing axis represents a potential strategy for modulating macrophage responses in autoimmune arthritis and aging-associated inflammation.

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Chitosan materials are much important in adsorption, separation and water treatment due to their hydrophilicity, biodegradability and easy functionalization. However, they were difficult to form structural materials, which limited its application in engineering. In this paper, a new type of chitosan porous materials was prepared with two-step strategy involving the freezing crosslinking of chitosan with glutaraldehyde to form cryogels, and their subsequent reduction with NaBH4 to transform CN bonds into CN bonds, resulting in remarkable improvement of mechanical property. That is, the strength remained almost unchanged after 80 % deformation. The abundant -NH2 and -OH on the surface of materials, as well as the unique pore structure from cryogels, gave relatively high adsorption capacity for metals and dyes (88.73 ± 4.25 mg·g-1 for Cu(II) and 3261.05 ± 36.10 mg·g-1 for Congo red). The surface hydrophilicity of materials made it possible for selective water permeation with over 95 % separation efficiency for oil-water mixtures. In addition, simple hydrophobic modification using bromotetradecane achieved selective oil permeation with over 96 % separation efficiency for oil-water mixtures. This study not only provides a new strategy to endow chitosan materials with excellent mechanical property, large adsorption capacity and good oil-water separation performance, but also offers environmentally friendly materials for sewage treatment applications.

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Poly(3,4-ethylenedioxythiophene):polystyrene sulfonate (PEDOT:PSS), a successfully commercialized polymeric semiconductor material, has potential as a transparent electrode in flexible electronic devices, yet has insufficient conductivity. We present the synthesis, properties, and directed crystallization of the PEDOT:dodecyl sulfate (PEDOT:DS) film. Iron(III) dodecyl sulfate (Fe(DS)3) multi-lamellar vesicles (MLVs), a new growth template, are used to synthesize and direct the growth of the PEDOT:DS film via vapor-phase polymerization of 3,4-ethylenedioxythiophene to form huge PEDOT:DS co-crystal domains within the MLV superstructure. The polycrystalline film has metallic conductivity (avg. ~1.0 × 104 S cm-1), is highly transparent and mechanically durable yet flexible, and suitable for next-generation flexible electronics. These noteworthy properties are conferred by the MLV lamellar superstructure of Fe(DS)3, a selective oxidant and an efficient in situ dopant that enhances the film hydrophobicity and durability. Sophisticated MLV-type oxidants are foreseen to enable the synthesis of more conductive, transparent, robust, flexible, and water-stable polymer electrode materials in future.

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With the rapid growth of data driven by high-throughput sequencing technologies, genomics has entered an era characterized by big data, which presents significant challenges for traditional bioinformatics methods in handling complex data patterns. At this critical juncture of technological progress, deep learning-an advanced artificial intelligence technology-offers powerful capabilities for data analysis and pattern recognition, revitalizing genomic research. In this review, we focus on four major deep learning models: Convolutional Neural Network(CNN), Recurrent Neural Network(RNN), Long Short-Term Memory(LSTM), and Generative Adversarial Network(GAN). We outline their core principles and provide a comprehensive review of their applications in DNA, RNA, and protein research over the past five years. Additionally, we also explore the use of deep learning in livestock genomics, highlighting its potential benefits and challenges in genetic trait analysis, disease prevention, and genetic enhancement. By delivering a thorough analysis, we aim to enhance precision and efficiency in genomic research through deep learning and offer a framework for developing and applying livestock genomic strategies, thereby advancing precision livestock farming and genetic breeding technologies.

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Due to high humification, hyperthermophilic composting products (HP) show potential for remediating heavy metal pollution. However, the interaction between HP and heavy metals remains unclear. This study investigated the adsorption mechanism and soil remediation effect of HP on heavy metals. The results showed that the maximum adsorption capacity of HP increased by an average of 30.74 % compared to conventional composting products. HP transformed 34.87 % of copper, 42.55 % of zinc, and 35.63 % of lead from exchangeable and reducible forms into residual and oxidizable forms, thus reducing the soil risk level. In conclusion, HP significantly enhanced the adsorption of heavy metals and their transformation from unstable to stable forms, primarily due to the higher content of hydroxyl and carboxyl groups. This study aims to demonstrate the effectiveness of HP for remediating heavy metal pollution and to enhance the understanding of the underlying mechanism, which lays a foundation for waste utilization.

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Here, we present a protocol for small interfering RNA (siRNA)-mediated U1 small nuclear RNA (snRNA) knockdown using fluorinated α-helical polypeptide in macrophages and mouse lungs, providing a dependable approach to silence U1 snRNA in vitro and in vivo. We describe steps for preparing P7F7/siRNA polyplexes and silencing U1 snRNA with P7F7/siRNA polyplexes in macrophages and mouse lungs. Knockdown efficiency is validated through reverse-transcription quantitative real-time PCR analysis. This protocol is applicable for studying the physiological or pathophysiological function of U1 snRNA. For complete details on the use and execution of this protocol, please refer to Zhang et al.1.

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Given the limitations of untargeted metabolomics in precise metabolite quantification, our current research employed a novel approach by integrating untargeted and targeted metabolomics utilizing ultra-high-performance liquid chromatography quadrupole time-of-flight tandem mass spectrometry (UHPLC-QTOF-MS/MS) to analyze the metabolic profile and potential biomarkers for tuberculosis (TB). A cohort of 36 TB patients and 36 healthy controls (HC) was enlisted to obtain serum samples. Multivariate pattern recognition and univariate statistical analysis were employed to screen and elucidate the differential metabolites, whereas dot plots and receiver operating characteristic (ROC) curves were established for the identification of potential biomarkers of TB. The results indicated a distinct differentiation between the two groups, identifying 99 metabolites associated with five primary metabolic pathways in relation to TB. Of these, 19 metabolites exhibited high levels of sensitivity and specificity, as evidenced by the area under curve values approaching 1. Following targeted quantitative analysis, three potential metabolites, namely, L-asparagine, L-glutamic acid, and arachidonic acid, were demonstrated excellent discriminatory ability as evidenced by the results of the ROC curve, dot plots, and random forest model. Particularly noteworthy was the enhanced diagnostic efficacy of the combination of these three metabolites compared to singular biomarkers, suggesting their potential utility as serum biomarkers for TB diagnosis.

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Arboviruses, transmitted by medical arthropods, pose a serious health threat worldwide. During viral infection, Post Translational Modifications (PTMs) are present on both host and viral proteins, regulating multiple processes of the viral lifecycle. In this study, a mammalian E3 ubiquitin ligase WWP2 (WW domain containing E3 ubiquitin ligase 2) is identified, which interacts with the NS1 protein of Zika virus (ZIKV) and mediates K63 and K48 ubiquitination of Lys 265 and Lys 284, respectively. WWP2-mediated NS1 ubiquitination leads to NS1 degradation via the ubiquitin-proteasome pathway, thereby inhibiting ZIKV infection in mammalian hosts. Simultaneously, it is found Su(dx), a protein highly homologous to host WWP2 in mosquitoes, is capable of ubiquitinating NS1 in mosquito cells. Unexpectedly, ubiquitination of NS1 in mosquitoes does not lead to NS1 degradation; instead, it promotes viral infection in mosquitoes. Correspondingly, the NS1 K265R mutant virus is less infectious to mosquitoes than the wild-type (WT) virus. The above results suggest that the ubiquitination of the NS1 protein confers different adaptations of ZIKV to hosts and vectors, and more importantly, this explains why NS1 K265-type strains have become predominantly endemic in nature. This study highlights the potential application in antiviral drug and vaccine development by targeting viral proteins' PTMs.

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Long non-coding RNAs (lncRNAs) are well known for their oncogenic or anti-oncogenic roles in cancer development. AGAP2-AS1, a new lncRNA, has been extensively demonstrated as an oncogenic lncRNA in various cancers. Abundant experimental results have proved the aberrantly high level of AGAP2-AS1 in a great number of malignancies, such as glioma, colorectal, lung, ovarian, prostate, breast, cholangiocarcinoma, bladder, colon and pancreatic cancers. Importantly, the biological functions of AGAP2-AS1 have been extensively demonstrated. It could promote the proliferation, migration and invasion of cancer cells. Simultaneously, the clinical significances of AGAP2-AS1 were also illustrated. AGAP2-AS1 was exceptionally overexpressed in various cancer tissues. Clinical studies disclosed that the abnormal overexpression of AGAP2-AS1 was tightly connected with overall survival (OS), lymph nodes metastasis (LNM), clinical stage, tumor infiltration, high histological grade (HG), serous subtype and PFI times. However, to date, the biological actions and clinical significances of AGAP2-AS1 have not been systematically reviewed in human cancers. In the present review, the authors overviewed the biological actions, potential mechanisms and clinical features of AGAP2-AS1 according to the previous studies. In summary, AGAP2-AS1, as a vital oncogenic gene, is a promising biomarker and potential target for carcinoma prognosis and therapy.

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Silicon-based material is regarded as one of the most promising anodes for next-generation high-performance lithium-ion batteries (LIBs) due to its high theoretical capacity and low cost. Harnessing silicon carbide's robustness, we designed a novel porous silicon with a sandwich structure of carbon/silicon carbide/Ag-modified porous silicon (Ag-PSi@SiC@C). Different from the conventional SiC interface characterized by a frail connection, a robust dual covalent bond configuration, dependent on SiC and SiOC, has been successfully established. Moreover, the innovative sandwich structure effectively reduces detrimental side reactions on the surface, eases volume expansion, and bolsters the structural integrity of the silicon anode. The incorporation of silver nanoparticles contributes to an improvement in overall electron transport capacity and enhances the kinetics of the overall reaction. Consequently, the Ag-PSi@SiC@C electrode, benefiting from the aforementioned advantages, demonstrates a notably elevated lithium-ion mobility (2.4 * 10-9 cm2·s-1), surpassing that of silicon (5.1 * 10-12 cm2·s-1). The half-cell featuring Ag-PSi@SiC@C as the anode demonstrated robust rate cycling stability at 2.0 A/g, maintaining a capacity of 1321.7 mAh/g, and after 200 cycles, it retained 962.6 mAh/g. Additionally, the full-cell, featuring an Ag-PSi@SiC@C anode and a LiFePO4 (LFP) cathode, exhibits outstanding longevity. Hence, the proposed approach has the potential to unearth novel avenues for the extended exploration of high-performance silicon-carbon anodes for LIBs.

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Long non-coding RNA (lncRNA) H19 is an extensively studied lncRNA that is related to numerous pathological changes. Our previous findings have documented that serum lncRNA H19 levels are decreased in patients with chronic kidney disorder and lncRNA H19 reduction is closely correlated with renal tubulointerstitial fibrosis, an essential step in developing end-stage kidney disease. Nonetheless, the precise function and mechanism of lncRNA H19 in renal tubulointerstitial fibrosis are not fully comprehended. The present work utilized a mouse model of unilateral ureteral obstruction (UUO) and transforming growth factor-ß1 (TGF-ß1)-stimulated HK-2 cells to investigate the possible role and mechanism of lncRNA H19 in renal tubulointerstitial fibrosis were investigated. Levels of lncRNA H19 decreased in kidneys of mice with UUO and HK-2 cells stimulated with TGF-ß1. Up-regulation of lncRNA H19 in mouse kidneys remarkably relieved kidney injury, fibrosis and inflammation triggered by UUO. Moreover, the increase of lncRNA H19 in HK-2 cells reduced epithelial-to-mesenchymal transition (EMT) induced by TGF-ß1. Notably, up-regulation of lncRNA H19 reduced lipid accumulation and triacylglycerol content in kidneys of mice with UUO and TGF-ß1-stimulated HK-2 cells, accompanied by the up-regulation of long-chain acyl-CoA synthetase 1 (ACSL1). lncRNA H19 was identified as a sponge of microRNA-130a-3p, through which lncRNA H19 modulates the expression of ACSL1. The overexpression of microRNA-130a-3p reversed the lncRNA H19-induced increases in the expression of ACSL1. The suppressive effects of lncRNA H19 overexpression on the EMT, inflammation and lipid accumulation in HK-2 cells were diminished by ACSL1 silencing or microRNA-130a-3p overexpression. Overall, the findings showed that lncRNA H19 ameliorated renal tubulointerstitial fibrosis by reducing lipid deposition via modulation of the microRNA-130a-3p/ACSL1 axis.

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BACKGROUND: The capacity of high-density lipoprotein cholesterol (HDL) to acquire free cholesterol (FC) from triglyceride-rich lipoproteins during lipoprotein lipase-dependent lipolysis in a process of reverse remnant cholesterol transport, has been proposed as a key biological function of HDL particles that underlies the U-shaped relationship between HDLcholesterol and cardiovascular diseases. Although reverse remnant cholesterol transport has been evaluated in a fasting state, it has never been explored under nonfasting conditions. METHODS AND RESULTS: FC transfer was evaluated in healthy men (n=78) before and throughout the postprandial phase up to 8 hours after consumption of a test meal. Postprandially, the capacity of HDL to acquire FC increased progressively, reaching a maximal mean value of 98.5%±22.5% 6 hours after meal intake (P<0.05). Analysis of the study population according to tertiles of postprandial variation of FC transfer identified subjects exhibiting reduced capacity of HDL to acquire FC (tertile 1), those for whom the capacity of HDL to acquire FC remained unchanged (tertile 2), and subjects characterized by an enhanced FC transfer during the postprandial phase (tertile 3). Across the tertiles, we found an inverse relationship between the maximal postprandial change in FC transfer to HDL and the degree of postprandial triglyceride response. CONCLUSIONS: Healthy individuals exhibiting exacerbated postprandial triglyceride response and reduced HDL cholesterol levels feature reduced FC transfer to HDL during the postprandial state. These data suggest that to normalize postprandial triglyceride response, 2 conditions need to be fulfilled: notably elevated FC transfer to HDL in the postprandial phase and increased levels of acceptor HDL particles.

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Aims/Background Prostate cancer stands out as one of the most prevalent malignant tumours among males. The non-invasive identification of clinically significant prostate cancer via magnetic resonance imaging plays a critical role in circumventing unnecessary biopsies and determining suitable treatment strategies for patients. Our study aimed to evaluate the potential improvement in predictive accuracy for clinically significant prostate cancer by incorporating perfusion data obtained from dynamic contrast-enhanced magnetic resonance imaging acquisition protocols into multiparametric magnetic resonance imaging parameters. Methods Radiomics extracted from perfusion parameters (Ktrans, Kep, Ve) of dynamic contrast-enhanced magnetic resonance imaging were analysed in patients suspected of prostate cancer who underwent 3T multiparametric magnetic resonance imaging between January 2017 and June 2023 in this retrospective study. The pathological findings obtained from biopsy or therapy were categorised into groups based on the Gleason sum score as either clinically significant prostate cancer (Gleason sum score > 7) or non-clinically significant prostate cancer (Gleason sum score ≤ 6). Diagnostic models were constructed using logistic regression analysis, incorporating prostate imaging reporting and data system V2.1 scores and clinical data, with or without radiomics extracted from dynamic contrast-enhanced. The area under curve (AUC) values were compared using the DeLong test. Results Overall, 214 men (clinically significant prostate cancer [n=78] and non-clinically significant prostate cancer [n=136]) were included. The clinical-prostate imaging reporting and data system model demonstrated an AUC of 0.89 (95% confidence interval: 0.84-0.95) in the training cohort and 0.91 (95% confidence interval: 0.84-0.98) in the test cohort. For the clinical-prostate imaging reporting and data system-radscore model, the AUC values were 0.97 (95% confidence interval: 0.95-0.99) for Ktrans, 0.98 (95% confidence interval: 0.96-1.00) for Ve, and 0.96 (95% confidence interval: 0.93-0.98) for Kep in the training cohort, and 0.97 (95% confidence interval: 0.94-1.00) for Ktrans, 0.95 (95% confidence interval: 0.91-1.00) for Ve, and 0.97 (95% confidence interval: 0.94-1.00) for Kep in the test cohort. Radiomics based on perfusion parameters exhibited good diagnostic performance in predicting clinically significant prostate cancer. The clinical-prostate imaging reporting and data system-radscore model demonstrated superior diagnostic capability compared to perfusion-based radiomics or clinical-prostate imaging reporting and data system models alone. Conclusion The application of radiomics, which involves extracting perfusion parameters from dynamic contrast-enhanced imaging, has the potential to enhance diagnostic accuracy for clinically significant prostate cancer.

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Background: Over-activated osteoclast (OC) is a major cause of diseases related to bone loss and bone metabolism. Both bone resorption inhibition and apoptosis induction of osteoclast are crucial in treating these diseases. X-linked inhibitor of apoptosis protein (XIAP)-associated factor 1 (XAF1) is an important interferon-stimulated and apoptotic gene. However, how XAF1 regulates bone formation and remodeling is unknown. Methods: We generate global and chimeric Xaf1 knockout mouse models and utilize these models to explore the function and mechanism of XAF1 in regulating bone formation and remodeling in vivo and in vitro. Results: We show that XAF1 depletion enhances osteoclast generation in vitro. XAF1 knockout increases osteoclast number and bone resorption, thereby exacerbating bone loss in both OVX and osteolysis models. Activation of XAF1 with BV6 (a potent XIAP inhibitor) suppresses osteoclast formation. Mechanistically, XAF1 deletion decreases osteoclast apoptosis by facilitating the interaction between XIAP and caspase-3/7. Conclusions: Our data illustrates an essential role of XAF1 in controlling osteoclastogenesis in both osteoporosis and osteolysis mouse models and highlights its underlying mechanism, indicating a potential role in clinical treatment.The translational potential of this article: The translation potential of this article is that we first indicated that osteoclast apoptosis induced by XAF1 contribute to the progression of osteoporosis and osteolysis, which provides a novel strategy in the prevention of osteoporosis and osteolysis.

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Oxidative stress plays a pivotal role in the development of diabetic cardiomyopathy (DCM). Previous studies have revealed that inhibition of mitochondrial fission suppressed oxidative stress and alleviated mitochondrial dysfunction and cardiac dysfunction in diabetic mice. However, no research has confirmed whether mitochondria fission accentuates hyperglycemia-induced cardiomyoblast oxidative stress through regulating fatty acid oxidation (FAO). We used H9c2 cardiomyoblasts exposed to high glucose (HG) 33 mM to simulate DCM in vitro. Excessive mitochondrial fission, poor cell viability, and lipid accumulation were observed in hyperglycemia-induced H9c2 cardiomyoblasts. Also, the cells were led to oxidative stress injury, lower adenosine triphosphate (ATP) levels, and apoptosis. Dynamin-related protein 1 (Drp1) short interfering RNA (siRNA) decreased targeted marker expression, inhibited mitochondrial fragmentation and lipid accumulation, suppressed oxidative stress, reduced cardiomyoblast apoptosis, and improved cell viability and ATP levels in HG-exposed H9c2 cardiomyoblasts, but not in carnitine palmitoyltransferase 1 (CPT1) inhibitor etomoxir treatment cells. We also found subcellular localization of CPT1 on the mitochondrial membrane, FAO, and levels of nicotinamide adenine dinucleotide phosphate (NADPH) were suppressed after exposure to HG treatment, whereas Drp1 siRNA normalized mitochondrial CPT1, FAO, and NADPH. However, the blockade of FAO with etomoxir abolished the above effects of Drp1 siRNA in hyperglycemia-induced H9c2 cardiomyoblasts. The preservation of mitochondrial function through the Drp1/CPT1/FAO pathway is the potential mechanism of inhibited mitochondria fission in attenuating oxidative stress injury of hyperglycemia-induced H9c2 cardiomyoblasts.

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Type I interferons (IFN-I) are pleiotropic factors endowed with multiple activities that play important roles in innate and adaptive immunity. Although many studies indicate that IFN-I inducers exert favorable effects on broad-spectrum antivirus, immunomodulation, and anti-tumor activities by inducing endogenous IFN-I and IFN-stimulated genes, their function in bone homeostasis still needs further exploration. Here, our study demonstrates 2 distinct IFN-I inducers, diABZI and poly(I:C), as potential therapeutics to alleviate osteolysis and osteoporosis. First, IFN-I inducers suppress the genes that control osteoclast (OC) differentiation and activity in vitro. Moreover, diABZI alleviates bone loss in Ti particle-induced osteolysis and ovariectomized -induced osteoporosis in vivo by inhibiting OC differentiation and function. In addition, the inhibitory effects of IFN-I inducers on OC differentiation are not observed in macrophages derived from Ifnar1-/-mice, which indicate that the suppressive effect of IFN-I inducers on OC is IFNAR-dependent. Mechanistically, RNAi-mediated silencing of IRF7 and IFIT3 in OC precursors impairs the suppressive effect of the IFN-I inducers on OC differentiation. Taken together, these results demonstrate that IFN-I inducers play a protective role in bone turnover by limiting osteoclastogenesis and bone resorption through the induction of OC-specific mediators via the IFN-I signaling pathway.

OCs are responsible for bone resorption, and their excessive differentiation and enhanced activity will lead to bone resorption diseases such as osteoporosis and osteolysis. Here, our study demonstrates 2 distinct IFN-I inducers, diABZI and poly(I:C), as potential therapeutics to alleviate osteolysis and osteoporosis. IFN-I inducers suppress OC differentiation, and particularly diABZI alleviates bone loss in osteolysis and osteoporosis mouse models. Taken together, IFN-I inducers play a protective role in bone turnover by limiting osteoclastogenesis and bone resorption through the induction of OC-specific mediators via the IFN-I signaling pathway. Our in-depth and comprehensive discovery of the IFN-I inducer would provide new insight into OC biology and therapeutic targets for osteoclastic bone resorption diseases.

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All-solid-state ionic conductive elastomers (ASSICEs) are emerging as a promising alternative to hydrogels and ionogels in flexible electronics. Nevertheless, the synthesis of ASSICEs with concomitant mechanical robustness, superior ionic conductivity, and cost-effective recyclability poses a formidable challenge, primarily attributed to the inherent contradiction between mechanical strength and ionic conductivity. Herein, we present a collaborative design of high-entropy topological network and multivalent ion-dipole interaction for ASSICEs, and successfully mitigate the contradiction between mechanical robustness and ionic conductivity. Benefiting from the synergistic effect of this design, the coordination, de-coordination, and intrachain transfer of Li+ are effectively boomed. The resultant ASSICEs display exceptional mechanical robustness (breaking strength: 7.45 MPa, fracture elongation: 2621%, toughness: 107.19 MJ m-3) and impressive ionic conductivity (1.15 × 10-2 S m-1 at 25 °C). Furthermore, these ASSICEs exhibit excellent environmental stability (fracture elongation exceeding 1400% at 50 °C or -60 °C) and recyclability. Significantly, the application of these ASSICEs in a strain sensor highlights their potential in various fields, including human-interface communication, aerospace vacuum measurement, and medical balloon monitoring.