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Solid oxide fuel cells (SOFCs) are vital for alternative energy, powering motors effi-ciently. They offer fuel versatility and waste heat recovery, making them ideal for various applications. Optimizing interconnector structures is crucial for SOFC advancement. This paper introduces a novel 2D simulation model for interconnector SOFCs, aiming to enhance their performance. We initially construct a single half-cell model for a conventional interconnector SOFC, ensuring model accuracy. Subsequently, we propose an innovative interconnector SOFC model, which outperforms the conventional counterpart in various aspects.

This study aimed to investigate the efficacy of pre-treatment with different concentrations of sufentanil in mitigating propofol injection-induced pain. This study included 421 patients who were scheduled for gastrointestinal endoscopy between June 2023 and December 2024. Participants were randomly assigned to one of the four groups with different concentrations sufentanil: 0 µg/mL group(0.9% normal saline), 0.5 µg/mL group, 1 µg/mL group and 5 µg/mL group. Among the four groups, the rates of pain relief were 82 (77.4%), 93 (89.4%), 96 (89.7%), and 91 (87.5%), respectively. Compared to the 0 µg/mL group, the other groups demonstrated significantly reduced pain following propofol injection (p < 0.05). The recovery times were 14.59 ± 3.92 min, 15.13 ± 3.20 min, 14.27 ± 3.06 min, and 15.57 ± 3.24 min, respectively. Notably, the 1 µg/mL group did not exhibit a prolonged recovery time compared to the 0 µg/mL group. The total propofol consumption was recorded as 218.5 ± 36.8 mg, 196.7 ± 31.0 mg, 183.8 ± 25.0 mg, and 189.6 ± 31.4 mg, respectively, with the 1 µg/mL group showing the lowest total propofol consumption among the groups. The incidences of adverse events (AEs) were 61.3%, 70.2%, 58.9%, and 76.9%, respectively. In comparison to the 1 µg/mL group, the 5 µg/mL group exhibited a higher incidence of AEs. Furthermore, multivariate analysis indicated that a 5 µg/mL dilution of sufentanil increases the risk of AEs (p < 0.05). The 1 µg/mL group demonstrated greater safety and efficacy when combined with propofol. The study has been registered in the Chinese Clinical Trial Registry (ChiCTR). Link of the registry: http://www.chictr.org.cn. Date of registration: 2023/06/12. Trial registration number: ChiCTR2300072402.

Wearable visual bionic devices, fueled by advancements in artificial intelligence, are making remarkable progress. However, traditional silicon vision chips often grapple with high energy losses and challenges in emulating complex biological behaviors. In this study, we constructed a van der Waals P3HT/GaAs nanowires P-N junction by carefully directing the arrangement of organic molecules. Combined with a Schottky junction, this facilitated multi-faceted birdlike visual enhancement, including broadband non-volatile storage, low-light perception, and a near-zero power consumption operating mode in both individual devices and 5 × 5 arrays on arbitrary substrates. Specifically, we realized over 5 bits of in-memory sensing and computing with both negative and positive photoconductivity. When paired with two imaging modes (visible and UV), our reservoir computing system demonstrated up to 94% accuracy for color recognition. It achieved motion and UV grayscale information extraction (displayed with sunscreen), leading to fusion visual imaging. This work provides a promising co-design of material and device for a broadband and highly biomimetic optoelectronic neuromorphic system. Traditional silicon vision chips often challenge in emulating complex biological behaviors. This work reports birdlike broadband neuromorphic visual sensor arrays with 5 bits of in-memory sensing and computing. The built reservoir computing system achieves motion and UV grayscale information extraction, leading to fusion visual imaging.

Perovskite light-emitting diodes (PeLEDs) have recently demonstrated great potential for next-generation displays. Fabricating PeLEDs by scalable and well-established thermal evaporation—the technique used for industrial manufacturing of organic light-emitting diodes—should accelerate the development of perovskite displays; however, thermal evaporation of perovskites produces films with a high density of defects due to fast and uncontrollable crystal growth during evaporation. As a result, the performance of evaporated PeLEDs is lagging behind their solution-processed counterparts. Here we develop a tri-source co-evaporation strategy to introduce a multifunctional Lewis-base additive that reduces the perovskite grain size while confining charge carriers and passivating surface defects. The process enables the in situ formation of high-quality perovskite nanocrystal films with improved crystallinity, enhanced photoluminescence quantum yield and suppressed defects. A peak external quantum efficiency of 16.4% is achieved for green PeLEDs with an all-thermally evaporated device architecture. We further fabricate active-matrix PeLED displays by integrating top-emitting PeLEDs on a 6.67-inch thin-film transistor backplane. The displays show high-definition images and videos with a resolution of 1,080 × 2,400 and continuous greyscale information. We anticipate that this work will stimulate the exploration of efficient vapour-deposited PeLEDs for industrial display applications.All-thermal evaporation enables the fabrication of green perovskite LEDs with a peak external quantum efficiency of 16.4%, and active-matrix displays with high resolution and continuous greyscale information.

Background: Diabetic neuropathic pain (DNP) is a common complication of diabetes with significant impact on patients’ quality of life. Current treatments have limitations, and exploring new mechanisms and targets is crucial. Objective Our study aims to explore the role and mechanism of circRNA_19601 (circ19601) in regulating miR-324-5p in DNP within the dorsal root ganglion (DRG). Methods: This study used streptozotocin (STZ) and high-fat diet-induced diabetic rat models, as well as high-sugar treated DRG neurons to construct cell models. The STZ and high-fat diet induced a diabetic neuropathic pain model in rats, and high-glucose conditions were used to extract DRG neurons. The effects of the positive control drug pregabalin on STZ rats were monitored under different dosing conditions by measuring body weight, blood glucose, mechanical paw withdrawal threshold, and thermal paw withdrawal latency. The study also analyzed the expression of circular RNA in DRG neurons affected by diabetic neuropathic pain. Next, we also examined the effects of knocking down circ19601 with or without the miR-324-5p inhibitor on DNP. The expression of pain-related membrane proteins was analyzed using Western blot. Results: STZ treatment in diabetic rats led to reduced body weight, elevated blood glucose, and decreased pain sensitivity. Pregabalin effectively improved mechanical hyperalgesia but mainly influenced mechanical sensitivity long-term. Transcriptomic analysis revealed upregulation of circ19601 in diabetic rats, which was reversed by pregabalin. Knockdown of circ19601 improved body weight, reduced blood glucose, and alleviated pain sensitivity by increasing miR-324-5p levels and decreasing neurotransmitter and pain-related protein levels. MiR-324-5p inhibition reversed these effects, highlighting its role in regulating pain pathways in diabetic neuropathy. Conclusion: Pregabalin mitigates mechanical and thermal pain in diabetic rats. It does so by reversing decreased pain thresholds and modifying the expression of circ19601. This, in turn, impacts miR-324-5p and pain-related proteins, leading to improvements in body weight and blood glucose levels.

Cell type-specific analysis is crucial for uncovering biological insights hidden in bulk tissue data, yet single-cell or single-nuclei approaches are often cost-prohibitive for large samples. We introduce EPIC-unmix, a novel two-step empirical Bayesian method combining reference single-cell/single-nuclei and bulk RNA-seq data to improve cell type-specific inference, accounting for the difference between reference and target datasets. Under comprehensive simulations, we demonstrate that EPIC-unmix outperforms alternative methods in accuracy. Applied to Alzheimer’s disease brain RNA-seq data, EPIC-unmix identifies multiple differentially expressed genes in a cell type-specific manner, and empowers cell type-specific eQTL analysis.

Background Smac mimetics are a type of drug that can induce apoptosis by antagonizing IAP family members in cancer treatment. However, a recent study showed that Smac mimetics can trigger cell invasion and migration in cancer cells by activating the NF-κB pathway. Methods We assessed lung cancer cell elongation, invasion and migration under treatment with the Smac mimetic LCL161. Functional analyses (in vitro and in vivo) were performed to detect the contribution of NIK and OTUD7B to LCL161-induced cell invasion and migration. The role of OTUD7B in regulation of the TRAF3/NIK/NF-κB pathway under LCL161 treatment was analysed by immunoblotting, immunoprecipitation, luciferase and ubiquitin assays, shRNA silencing and plasmid overexpression. Expression levels of OTUD7B, NIK and TRAF3 in tissue samples from lung cancer patients were examined by immunohistochemistry. Results We found that LCL161 stimulates lung cancer cell elongation, invasion and migration at non-toxic concentrations. Mechanistically, LCL161 results in NIK accumulation and activates the non-canonical rather than the canonical NF-κB pathway to enhance the transcription of target genes, such as IL-2 and MMP-9. Importantly, knockdown of NIK dramatically suppresses LCL161-induced cell invasion and migration by reducing the proteolytic processing of p100 to p52 and target gene transcription. Interestingly, we discovered that OTUD7B increases TRAF3 and decreases NIK to inhibit the non-canonical NF-κB pathway and that overexpression of OTUD7B suppresses LCL161-induced cell invasion and migration. Notably, OTUD7B directly binds to TRAF3 rather than to NIK and deubiquitinates TRAF3, thereby inhibiting TRAF3 proteolysis and preventing NIK accumulation and NF-κB pathway activation. Furthermore, the OTU domain of OTUD7B is required for the inhibition of LCL161-induced cell invasion and migration, as demonstrated by transfection of the C194S/H358R(CH) mutant OTUD7B. Finally, we investigated whether OTUD7B inhibits LCL161-induced lung cancer cell intrapulmonary metastasis in vivo, and our analysis of clinical samples was consistent with the above findings. Conclusions Our study highlights the importance of OTUD7B in the suppression of LCL161-induced lung cancer cell invasion and migration, and the results are meaningful for selecting lung cancer patients suitable for LCL161 treatment.

Novel MoAlB composites reinforced with 5–15 vol% SiC have been firstly prepared and characterized in the present study. The SiC reinforcement is stable with MoAlB at a sintering temperature of 1200 °C in Ar. The 5 vol% SiC/MoAlB composite exhibited improved mechanical properties and enhanced oxidation resistance. A flexural strength of 380 MPa and a Vickers hardness of 12.7 GPa were achieved and increased by 24% and 51%, respectively, as compared with those for MoAlB, indicating the enhanced strengthening effect of SiC. Cyclic oxidation tests at 1200 and 1300 °C for 10 h in air showed that the 5 vol% SiC/MoAlB composite has better oxidation resistance than MoAlB due to the formation of a dense and continuous scale composed of Al 2 O 3 and SiO 2 , which prevents the oxygen inward diffusion and the evaporation of oxides. We expect that the general strategy of second phase reinforcing for materials will help to widen the applications of MoAlB composites.

The cytokine IL-15 mediates development and survival of immune cells, including natural killer T (NKT) cells, but the underlying mechanism of IL-15 function is incompletely understood. Here we show that IL-15 induces autophagy in NKT cells with a mechanism that involves a crucial signaling component, TBK-binding protein 1 (Tbkbp1). Tbkbp1 facilitates activation of the autophagy-initiating kinase Ulk1 through antagonizing the inhibitory action of mTORC1. This antagonization involves the recruitment of an mTORC1-opposing phosphatase to Ulk1. Tbkbp1 deficiency attenuates IL-15-stimulated NKT cell autophagy, and is associated with mitochondrial dysfunction, aberrant ROS production, defective Bcl2 expression and reduced NKT cell survival. Consequently, Tbkbp1-deficient mice have profound deficiency in NKT cells, especially IFN-γ-producing NKT1. We further show that Tbkbp1 regulates IL-15-stimulated autophagy and survival of NK cells. These findings suggest a mechanism of autophagy induction by IL-15, and establish Tbkbp1 as a regulator of NKT cell development and survival. Interleukin-15 (IL-15) regulates the homeostasis of many immune cell types, including natural killer T (NKT) cells, but the underlying mechanism is not completely clear. Here the authors analyse Tbkbp1 -deficient mice and show that IL-15 induces Tbkbp1-dependent autophagy to modulate NKT survival.

Glioblastoma multiforme (GBM), the most aggressive primary brain tumor, is associated with extremely poor patient prognosis. Temozolomide (TMZ) resistance remains a major cause of treatment failure. Protein arginine methyltransferase 6 (PRMT6) plays critical roles in tumorigenesis, but its function and regulatory mechanisms in GBM TMZ resistance have not been elucidated. While the hypoxic microenvironment is a hallmark feature of GBM, its epigenetic regulatory mechanisms in drug resistance remain unclear. We analyzed PRMT6 expression and prognostic value in GBM using public databases (TCGA, CGGA). TMZ resistance was assessed through in vitro assays (CCK-8, flow cytometry, colony formation) and in vivo xenograft models. Molecular mechanisms of the HIF-1α/PRMT6/G3BP1 axis were investigated via RNA sequencing, ChIP-qPCR, dual-luciferase reporter assays, and co-immunoprecipitation. PRMT6 was highly expressed in GBM and correlated with poor prognosis. Hypoxia transcriptionally activated PRMT6 through HIF-1α. Elevated PRMT6 expression promoted TMZ resistance, while its knockdown enhanced drug sensitivity. Mechanistically, PRMT6 interacted with transcription factor GABPA to upregulate stress granule core protein G3BP1, subsequently suppressing pro-apoptotic BCL2L13 and conferring chemoresistance. In vivo studies confirmed that both PRMT6 and G3BP1 significantly influenced TMZ resistance. This study provides evidence that hypoxia mediates TMZ resistance in GBM through the HIF-1α/PRMT6/G3BP1 axis, identifying PRMT6 and G3BP1 as promising therapeutic targets to overcome chemoresistance.