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Sigma‐1 receptor (S1R) regulates reactive oxygen species (ROS) accumulation via nuclear factor erythroid 2‐related factor 2 (NRF2), which plays a vital role in ferroptosis. Sorafenib is a strong inducer of ferroptosis but not of apoptosis. However, the mechanism of sorafenib‐induced ferroptosis in hepatocellular carcinoma (HCC) remains unclear. In this study, we found for the first time that sorafenib induced most of S1Rs away from nucleus compared to control groups in Huh‐7 cells, and ferrostatin‐1 completely blocked the translocation. S1R protein expression, but not mRNA expression, in HCC cells was significantly up‐regulated by sorafenib. Knockdown of NRF2, but not of p53 or hypoxia‐inducible factor 1‐alpha (HIF1α), markedly induced S1R mRNA expression in HCC cells. Inhibition of S1R (by RNAi or antagonists) increased sorafenib‐induced HCC cell death in vitro and in vivo. Knockdown of S1R blocked the expression of glutathione peroxidase 4 (GPX4), one of the core targets of ferroptosis, in vitro and in vivo. Iron metabolism and lipid peroxidation increased in the S1R knockdown groups treated with sorafenib compared to the control counterpart. Ferritin heavy chain 1 (FTH1) and transferrin receotor protein 1 (TFR1), both of which are critical for iron metabolism, were markedly up‐regulated in HCC cells treated with erastin and sorafenib, whereas knockdown of S1R inhibited these increases. In conclusion, we demonstrate that S1R protects HCC cells against sorafenib and subsequent ferroptosis. A better understanding of the role of S1R in ferroptosis may provide novel insight into this biological process.

Influenza A virus (IAV) infection initiates a complex interplay of cell death modalities, including apoptosis, necroptosis, pyroptosis, and their integration, known as PANoptosis, which significantly impacts host immune responses and tissue integrity. These pathways are intricately regulated by viral proteins and host factors, contributing to both viral clearance and pathogenesis-related tissue damage. This review comprehensively explores the molecular mechanisms underlying these cell death processes in influenza infection. We highlight the roles of key regulatory proteins, such as ZBP1 (Z-DNA binding protein 1) and RIPK3 (receptor-interacting protein kinase 3), in orchestrating these responses, emphasizing the dual roles of cell death in both antiviral defense and tissue injury. Furthermore, we discuss emerging therapeutic strategies targeting these pathways, aiming to enhance antiviral efficacy while minimizing collateral tissue damage. Future research should focus on targeted approaches to modulate cell death mechanisms, aiming to reduce tissue damage and improve clinical outcomes for patients with severe influenza.

The rapid development of the new energy vehicle (NEV) industry has led to concerns about battery quality and the transparency of green recycling, causing uncertainty among consumers. Many firms adopt blockchain technology to solve this problem, but blockchain adoption will bring privacy leakage risk to consumers. A Stackelberg game model of a three stage NEV supply chain is constructed to examine the impact of adapting blockchain on strategic decisions of supply chain participants. We consider a setting in which a battery supplier provides batteries to a NEV manufacturer, and a third-party recycler recovers retired batteries for a NEV manufacturer. We explore the influence of consumers’ green recycling preferences on the decisions of NEV supply chain members in three scenarios: not adopting blockchain traceability (NB), adopting blockchain with forward traceability (FB), and adopting blockchain with forward–reverse traceability (DB). We find that NEV supply chain members are more likely to adopt forward–reverse traceability under certain conditions. Moreover, the adoption of blockchain drives the battery supplier and NEV manufacture to increase wholesale price and retail price, especially under forward–reverse traceability. In addition, when consumers exhibit strong preferences for green recycling, third-party recyclers are more willing to invest in blockchain-based recycling due to its ability to enhance the accuracy and credibility of recycling data.

Salmonella is a foodborne pathogen that enters the host’s body through contaminated food and water, leading to gastroenteritis and systemic diseases. It is a significant veterinary and human pathogen capable of infecting both humans and animals, with substantial impacts on public health, human well-being, and the economic development of the livestock and poultry farming industry. Small non-coding RNAs (sRNAs), typically 50–500 nucleotides (nt) in length, have been identified in various bacteria, including Escherichia coli , Brucella , Pseudomonas aeruginosa , and Salmonella . These sRNAs play crucial roles in regulating diverse physiological processes within bacteria. This review emphasizes recent advances in understanding how sRNAs regulate the virulence of Salmonella spp, such as the discovery of novel sRNAs like SaaS and new regulatory mechanisms of known sRNAs like RyhB-1/RyhB-2 and SdsR/Spot 42. It also outlines critical future directions, including exploring the multifaceted functions of sRNAs in lifestyle or infection phase transitions, fully elucidating their roles in regulating the host immune response, studying the combined actions of multiple sRNAs on host pathogenesis and expanding research to more Salmonella serotypes and diverse animal models. Through these efforts, this review aims to enhance our understanding of Salmonella sRNAs and their infection mechanisms.

As China’s second largest energy-use sector, residential consumption has a great potential for carbon dioxide (CO2) reduction and energy saving or transition. Thus, here, using the methods of social network analysis (SNA) and geographically weighted regression (GWR), we investigated the spatiotemporal evolution characteristics of China’s residential CO2 emissions (RCEs) from direct energy use and proposed some policy suggestions for regional energy transition. (1) From 2000 to 2019, the total direct RCEs rose from 396.32 Mt to 1411.69 Mt; the consumption of electricity and coal were the primary sources. Controlling coal consumption and increasing the proportion of electricity generated from renewable energy should be the effective way of energy transition. (2) The spatial associations of direct RCEs show an obvious spatial network structure and the number of associations is increasing. Provinces with a higher level of economic development (Beijing, Shanghai, and Jiangsu) were at the center of the network and classified as the net beneficiary cluster in 2019. These provinces should be the priority areas of energy transition. (3) The net spillover cluster (Yunnan, Shanxi, Xinjiang, Gansu, Qinghai, Guizhou) is an important area to develop clean energy. People in this cluster should be encouraged to use more renewable energy. (4) GDP and per capita energy consumption had a significant positive influence on the growth of direct RCEs. Therefore, the national economy should grow healthily and sustainably to provide a favorable economic environment for energy transition. Meanwhile, residential consumption patterns should be greener to promote the use of clean energy.

Infection and replication of enveloped viruses require host cells to supply substantial amounts of cellular cholesterol for processes such as binding, entry, trafficking, assembly, and budding. However, the mechanisms by which influenza A virus (IAV) regulates cholesterol biosynthesis remain poorly understood. In this study, we demonstrate that IAV infection induces the expression of the retinoic acid-related orphan receptor γ (RORγ), an orphan nuclear receptor, which cooperates with the sterol regulatory element-binding protein-2 (SREBP2) to regulate the expression of the 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase (HMGCR), a key enzyme in cholesterol biosynthesis. RORγ knockout and treatment with two RORγ inhibitors, XY018 and GSK805, suppress IAV-induced HMGCR expression, cholesterol biosynthesis, and viral replication. Notably, exogenous cholesterol rescues the inhibitory effect of XY018 on viral replication. Mechanistically, we show that IAV infection activates RORγ expression through the TGF-β-activated kinase 1 (TAK1) and its downstream kinases, the c-Jun N-terminal kinase (JNK) and the IκB kinase (IKK), which in turn activate AP1 and NF-κB. In vivo, RORγ knockout reduces IAV replication, alleviates body weight loss, and prolongs survival in infected mice. Furthermore, XY018 treatment reduces both viral replication and inflammation in the lungs of IAV-infected mice. Our findings provide novel mechanistic insights into how IAV infection upregulates cholesterol biosynthesis to facilitate viral replication.

Many DNA viruses develop various strategies to inhibit cell death to facilitate their replication. However, whether influenza A virus (IAV), a fast-replicating RNA virus, attenuates cell death remains unknown. Here, we report that IAV infection induces TAK1 phosphorylation in a murine alveolar epithelial cell line (LET1) and a murine fibroblastoma cell line (L929). The TAK1-specific inhibitor 5Z-7-Oxzeneonal (5Z) and TAK1 knockout significantly enhance IAV-induced apoptosis, as evidenced by increased PARP, caspase-8, and caspase-3 cleavage. TAK1 inhibition also increases necroptosis as evidenced by increased RIPK1 S166 , RIPK3 T231/S232 , and MLKL S345 phosphorylation. Mechanistically, TAK1 activates IKK, which phosphorylates RIPK1 S25 and inhibits its activation. TAK1 also activates p38 and its downstream kinase MK2, which phosphorylates RIPK1 S321 but does not affect RIPK1 activation. Further investigation revealed that the RIPK1 inhibitor Nec-1 and RIPK1 knockout abrogate IAV-induced apoptosis and necroptosis; re-expression of wild-type but not kinase-dead (KD)-RIPK1 restores IAV-induced cell death. ZBP1 knockout abrogates IAV-induced cell death, whereas RIPK3 knockout inhibits IAV-induced necroptosis but not apoptosis. 5Z treatment enhances IAV-induced cell death and slightly reduces the inflammatory response in the lungs of H1N1 virus-infected mice and prolongs the survival of IAV-infected mice. Our study provides evidence that IAV activates TAK1 to suppress RIPK1-dependent apoptosis and necroptosis, and that RIPK3 is required for IAV-induced necroptosis but not apoptosis in epithelial cells.

Rheumatoid arthritis (RA) is a chronic and inflammatory autoimmune disease. Macrophage pyroptosis, a proinflammatory form of cell death, is critically important in RA; however, the detailed mechanism underlying pyroptosis induction is not yet well understood. Here, we report that DNA polymerase β (Pol β), a key enzyme in base excision repair, plays a pivotal role in RA pathogenesis. Our data shows that Pol β expression is significantly decreased in peripheral blood mononuclear cells (PBMCs) from active RA patients and collagen-induced arthritis (CIA) mice, and Pol β deficiency increases the incidence of RA, macrophage infiltration, and bone destruction in CIA mouse models. In vitro, experiments showed that Pol β deficiency exacerbated macrophage pyroptosis induced by LPS plus ATP, while overexpression of Pol β inhibited macrophage pyroptosis. Further characterization revealed that Pol β knockout resulted in DNA damage accumulation and cytosolic dsDNA leakage, which activated the cGAS-STING-NF-κB signaling pathway and upregulated the expression of NLRP3, IL-1 β, and IL-18. In conclusion, our findings clarify the influence of Pol β on the development of RA and provide a detailed explanation for the STING-NF-κB pathway to induce macrophage pyroptosis.

In order to solve the interface issues in solution deposition of multilayer OLED devices, a blended host concept was developed and applied to both spin-coating and inkjet printing of phosphorescent OLEDs. The blended host consists of 1,3-bis(carbazolyl)benzene (mCP) and1,3,5-tri(phenyl-2-benzimidazoly)-benzene (TPBi). Maximum current efficiency (CE) of 24.2 cd A −1 and external quantum efficiency (EQE) of 7.0% have been achieved for spin-coated device. Maximum CE and EQE of 23.0 cd A −1 and 6.7% have been achieved for inkjet printed device. The films deposited by printing and spin-casting were further researched to explore the effect of those different processing methods on device performance.

Blockchain technology allows fresh agricultural enterprises to share records stored on the chain, and the technology can benefit information management systems, such as decentralization and transparency. This study uses game theory to examine a blockchain introduction strategy for fresh agricultural enterprises in a competitive environment, considering consumer traceability preferences. We establish a pricing decision model in traditional and blockchain traceability modes and identify optimal solutions. Additionally, we analyze the impact of the blockchain introduction strategy, consumer preferences, and blockchain influence factor on optimal pricing decisions. The results indicate that the introduction of blockchain could improve the profits of enterprises under certain conditions. Moreover, consumer traceability preferences and the blockchain influence factor could significantly affect the blockchain introduction strategy. We also discover that when the blockchain influence factor meets a certain range, introducing blockchain technique in the traceability system could shift demand from traditional enterprises to blockchain enterprises. The total market demand for blockchain enterprises under the blockchain traceability mode will increase, whereas that of traditional enterprises under the blockchain traceability mode will decrease. Both consumer traceability preferences and the blockchain influence factor could significantly affect optimal pricing. Finally, some management suggestions are provided for the traceability of fresh agricultural enterprises based on the research conclusions.