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Background Perioperative neurocognitive disorders (PND) with a high incidence frequently occur in elderly surgical patients closely associated with prolonged anesthesia-induced neurotoxicity. The neuromorphopathological underpinnings of anesthesia-induced neurotoxicity have remained elusive. Methods Prolonged anesthesia with sevoflurane was used to establish the sevoflurane-induced neurotoxicity (SIN) animal model. Morris water maze, elevated plus maze, and open field test were employed to track SIN rats’ cognitive behavior and anxiety-like behaviors. We investigated the neuropathological basis of SIN through techniques such as transcriptomic, electrophysiology, molecular biology, scanning electron microscope, Golgi staining, TUNEL assay, and morphological analysis. Our work further clarifies the pathological mechanism of SIN by depleting microglia, inhibiting neuroinflammation, and C1q neutralization. Results This study shows that prolonged anesthesia triggers activation of the NF-κB inflammatory pathway, neuroinflammation, inhibition of neuronal excitability, cognitive dysfunction, and anxiety-like behaviors. RNA sequencing found that genes of different types of synapses were downregulated after prolonged anesthesia. Microglial migration, activation, and phagocytosis were enhanced. Microglial morphological alterations were also observed. C1qa, the initiator of the complement cascade, and C3 were increased, and C1qa tagging synapses were also elevated. Then, we found that the “Eat Me” complement pathway mediated microglial synaptic engulfment in the hippocampus after prolonged anesthesia. Afterward, synapses were remarkably lost in the hippocampus. Furthermore, dendritic spines were reduced, and their genes were also downregulated. Depleting microglia ameliorated the activation of neuroinflammation and complement and rescued synaptic loss, cognitive dysfunction, and anxiety-like behaviors. When neuroinflammatory inhibition or C1q neutralization occurred, complement was also decreased, and synaptic elimination was interrupted. Conclusions These findings illustrated that prolonged anesthesia triggered neuroinflammation and complement-mediated microglial synaptic engulfment that pathologically caused synaptic elimination in SIN. We have demonstrated the neuromorphopathological underpinnings of SIN, which have direct therapeutic relevance for PND patients.

The global push for low-carbon growth highlights the urgent need to examine how corporate internationalization shapes environmental performance. However, the environmental implications of corporate two-way foreign direct investment (CTFDI, integrating inward and outward FDI) remain insufficiently explored. This study investigates whether CTFDI mitigates corporate pollution emissions in line with the pollution halo hypothesis. This study employs a multiple fixed-effects OLS model using 43,410 firm-year observations from 2,894 A-share listed Chinese firms over 2008–2022. The results indicate that CTFDI significantly reduces emissions, with a one-unit increase associated with an average 0.15% decline. Mechanism analysis demonstrates that research and development investment and the adoption of digital and intelligent technologies are primary channels through which CTFDI exerts this effect. Heterogeneity analysis further reveals that non-state-owned enterprises and firms in non-polluting industries experience more pronounced benefits. Overall, the findings provide robust empirical evidence supporting the pollution halo hypothesis from the perspective of two-way FDI and highlight the role of economic openness in advancing green corporate development.

Background/Aims: Neurotoxic A1 astrocytes are induced by inflammation after spinal cord injury (SCI), and the inflammation-related Nuclear Factor Kappa B (NFκB) pathway may be related to A1-astrocyte activation. Mesenchymal stem cell (MSC) transplantation is a promising therapy for SCI, where transplanted MSCs exhibit anti-inflammatory effects by downregulating proinflammatory factors, such as Tumor Necrosis Factor (TNF)-α and NFκB. MSC-exosomes (MSC-exo) reportedly mimic the beneficial effects of MSCs. Therefore, in this study, we investigated whether MSCs and MSC-exo exert inhibitory effects on A1 astrocytes and are beneficial for recovery after SCI. Methods: The effects of MSC and MSC-exo on SCIinduced A1 astrocytes, and the potential mechanisms were investigated in vitro and in vivo using immunofluorescence and western blot. In addition, we assessed the histopathology, levels of proinflammatory cytokines and locomotor function to verify the effects of MSC and MSC-exo on SCI rats. Results: MSC or MSC-exo co-culture reduced the proportion of SCIinduced A1 astrocytes. Intravenously-injected MSC or MSC-exo after SCI significantly reduced the proportion of A1 astrocytes, the percentage of p65 positive nuclei in astrocytes, and the percentage of TUNEL-positive cells in the ventral horn. Additionally, we observed decreased lesion area and expression of TNFα, Interleukin (IL)-1α and IL-1β, elevated expression of Myelin Basic Protein (MBP), Synaptophysin (Syn) and Neuronal Nuclei (NeuN), and improved Basso, Beattie & Bresnahan (BBB) scores and inclined-plane-test angle. In vitro assay showed that MSC and MSC-exo reduced SCI-induced A1 astrocytes, probably via inhibiting the nuclear translocation of the NFκB p65. Conclusion: MSC and MSC-exo reduce SCI-induced A1 astrocytes, probably via inhibiting nuclear translocation of NFκB p65, and exert antiinflammatory and neuroprotective effects following SCI, with the therapeutic effect of MSCexo comparable with that of MSCs when applied intravenously.

This study explores the identity tensions and emotion regulation strategies of Chinese novice EFL teachers as they navigate these challenges. Using purposeful sampling, six novice EFL teachers were recruited based on their years of teaching experience, grade levels taught, and Banzhuren (homeroom teacher) experience. Data was collected through semi-structured interviews. Thematic analysis of the data reveals that identity tensions arise at the micro, meso, and macro levels, with emotion regulation playing a vital role in addressing these tensions. Participants’ imagined identity as key teachers in main subjects, collaborators with parents, and focused English teachers often conflict with the practiced identities as marginalised teachers, sole educators and constrained subordinate workers. Additionally, by applying Gross’s (2015) framework of emotion regulation, the research identifies four interrelated strategies that teachers employ to resolve identity tensions: cognitive reappraisal, situation modification, response modulation and attentional deployment. These strategies enable Chinese novice EFL teachers to either uphold their imagined identities, conform to their practiced identities, or, more frequently, inhabit a dynamic, transitional space between the two. The study broadens the understanding of EFL teachers’ professional identity development, highlighting the dynamic relationship between identity formation and emotion regulation.

Pain imposes a significant urden on patients, affecting them physically, psychologically, and economically. Despite numerous studies on the pathogenesis of pain, its clinical management remains suboptimal, leading to the under-treatment of many pain patients. Recently, research on the role of macrophages in pain processes has been increasing, offering potential for novel therapeutic approaches. Macrophages, being indispensable immune cells in the innate immune system, exhibit remarkable diversity and plasticity. However, the majority of research has primarily focused on the contributions of M1 macrophages in promoting pain. During the late stage of tissue damage or inflammatory invasion, M1 macrophages typically transition into M2 macrophages. In recent years, growing evidence has highlighted the role of M2 macrophages in pain relief. In this review, we summarize the mechanisms involved in M2 macrophage polarization and discuss their emerging roles in pain relief. Notably, M2 macrophages appear to be key players in multiple endogenous pathways that promote pain relief. We further analyze potential pathways through which M2 macrophages may alleviate pain.

Myocardial fibrosis (MF) is a common pathological feature of many heart diseases and seriously threatens the normal activity of the heart. Jiaogulan (Gynostemma pentaphyllum) tea is a functional food that is commercially available worldwide. Gypensapogenin I (Gyp I), which is a novel dammarane-type saponin, was obtained from the hydrolysates of total gypenosides. It has been reported to exert a beneficial anti-inflammatory effect. In our study, we attempted to investigate the efficiency and possible molecular mechanism of Gyp I in cardiac injury treatment induced by ISO. In vitro, Gyp I was found to increase the survival rate of H9c2 cells and inhibit apoptosis. Combined with molecular docking and Western blot analysis, Gyp I was confirmed to regulate the TLR4/NF-κB/NLRP3 signaling pathway. In vivo, C57BL6 mice were subcutaneously injected with 10 mg/kg ISO to induce heart failure. Mice were given a gavage of Gyp I (10, 20, or 40 mg/kg/d for three weeks). Pathological alterations, fibrosis-, inflammation-, and apoptosis-related molecules were examined. By means of cardiac function detection, biochemical index analysis, QRT-PCR monitoring, histopathological staining, immunohistochemistry, and Western blot analysis, it was elucidated that Gyp I could improve cardiac dysfunction, alleviate collagen deposition, and reduce myocardial fibrosis (MF). In summary, we reported for the first time that Gyp I showed good myocardial protective activity in vitro and in vivo, and its mechanism was related to the TLR4/NF-κB/NLRP3 signaling pathway.

Based on the China Family Panel Studies (CFPS) data from 2012 to 2022, this study systematically investigates the impact of household structure changes on consumption inequality and its underlying mechanisms. Against the backdrop of China’s economic transformation and demographic transition, the study integrates the Recentered Influence Function (RIF) regression with the RIF–Oaxaca–Blinder decomposition to identify the unconditional marginal effects of different household structure types—including six categories such as single-person households, compound households, and couple-only nuclear households—on consumption inequality. It further reveals the relative contributions of compositional (structural) and behavioral (coefficient) effects to the evolution of inequality. The findings show that the diversification of household structures has significantly intensified consumption inequality, particularly in high-level consumption categories such as healthcare, culture, education, and entertainment. Income and wealth disparities serve as the main amplification channels, while differences in saving behavior reflect unequal risk-sharing capacities. The heterogeneity analysis reveals that the inequality-enhancing effect of household structural changes is more pronounced among urban households, insured households, and those in the eastern and central regions. Dynamic decomposition results further demonstrate that the widening of consumption inequality is primarily driven by behavioral effects rather than compositional shifts. Overall, from a micro-behavioral perspective, this study uncovers the transmission mechanisms through which household structure changes amplify consumption inequality, providing new theoretical insights and empirical evidence for understanding consumption stratification and promoting inclusive upgrading amid demographic transition. How Household Structure Shapes Spending Inequality in China This study examines how changes in household structure have influenced household consumption inequality amid China’s rapid economic transformation and demographic transition. Using nationally representative panel data from 2012 to 2022, the results show that as single-person, couple-only, and multi-generational households have become more prevalent, consumption disparities across households have widened significantly. The analysis reveals that household structure affects consumption inequality primarily through three channels—income, wealth, and savings. Households with fewer members or weaker risk-sharing mechanisms tend to face unstable income sources, limited asset accumulation, and lower capacity for risk diversification, thereby amplifying consumption gaps. The study further finds notable heterogeneity across groups. The structural effects are more pronounced among urban households, insured households, and those in the eastern and central regions. In addition, dynamic decomposition results indicate that the widening of consumption inequality is mainly driven by growing differences in household consumption behaviors rather than changes in structural composition. This suggests that inequality has increased largely due to divergence in consumption preferences, saving decisions, and expenditure allocations across household types, rather than shifts in household structure shares. Overall, the findings demonstrate that demographic and structural transitions—rather than income growth alone—are key drivers of rising consumption inequality. By uncovering the micro-level mechanisms through which household structure shapes consumption disparities, this study provides valuable insights for designing inclusive social and economic policies that enable diverse household types to participate in and share the benefits of China’s high-quality development.

Glial fibrillary acidic protein (GFAP) has been suggested as a biomarker for reactive astrogliosis. We measured the levels of plasma GFAP by Simoa in 60 patients with PD with normal cognition, 63 with mild cognitive impairment (PD-MCI), 24 with dementia (PDD) and 15 healthy controls. A subgroup of patients with PD-MCI ( n  = 31) was followed up for 4.1 ± 2.3 years. Compared with healthy controls, plasma GFAP levels were elevated in patients with PDD (adjusted P  < 0.001) and PD-MCI (adjusted P  = 0.013) and were negatively correlated with the Mini Mental State Examination (MMSE) score in PD participants. Plasma GFAP predicted MCI-to-dementia conversion with an AUC of 0.90, higher than NfL, Tau and pTau181. Our results support that plasma GFAP has potential value for distinguishing patients with PDD, and predicting MCI-to-dementia conversion in PD.

High temperature stress poses a significant threat to the normal growth of maize seedlings, and key heat-resistant gene mining is the molecular basis for breeding new heat-resistant maize varieties. Through transcriptome sequencing of heat-tolerant hybrid ZD819 and its parental lines (ZD819-F, ZD819-M) under high-temperature stress, we identified 12 HSF (Heat shock transcription factors, HSFs) transcription factors from 12,442 differentially expressed genes. The results indicate that the maize hybrid ZD819 has stronger heat tolerance compared to its parent varieties (ZD819-F, ZD819-M). Transcriptome data identified 12 HSFs transcription factors, among which ZmHSF10 had the highest differential expression fold of 1279.40 before and after high-temperature treatment. The heat tolerance function of ZmHSF10 was studied by creating Arabidopsis thaliana materials overexpressing ZmHSF10 and obtaining ZmHSF10 silenced maize materials using VIGS technology. Genetic experiments have shown that overexpression of ZmHSF10 can stabilize the cell membrane stability of Arabidopsis plants under high temperature stress and improve their survival rate under high temperature treatment. Reducing the expression level of ZmHSF10 leads to a decrease in chlorophyll content, poor cell membrane stability, and lower relative water content in maize leaves under high temperature stress. These results preliminarily demonstrate that ZmHSF10 plays an important role in regulating heat tolerance in plants, providing genetic resources for enhancing heat tolerance in maize seedlings.

Dysfunction of the gap junction channel protein connexin 43 (Cx43) contributes to myocardial ischemia/reperfusion (I/R)-induced ventricular arrhythmias. Cx43 can be regulated by small ubiquitin-like modifier (SUMO) modification. Protein inhibitor of activated STAT Y (PIASy) is an E3 SUMO ligase for its target proteins. However, whether Cx43 is a target protein of PIASy and whether Cx43 SUMOylation plays a role in I/R-induced arrhythmias are largely unknown. Male Sprague-Dawley rats were infected with PIASy short hairpin ribonucleic acid (shRNA) using recombinant adeno-associated virus subtype 9 (rAAV9). Two weeks later, the rats were subjected to 45 min of left coronary artery occlusion followed by 2 h reperfusion. Electrocardiogram was recorded to assess arrhythmias. Rat ventricular tissues were collected for molecular biological measurements. Following 45 min of ischemia, QRS duration and QTc intervals statistically significantly increased, but these values decreased after transfecting PIASy shRNA. PIASy downregulation ameliorated ventricular arrhythmias induced by myocardial I/R, as evidenced by the decreased incidence of ventricular tachycardia and ventricular fibrillation, and reduced arrythmia score. In addition, myocardial I/R statistically significantly induced PIASy expression and Cx43 SUMOylation, accompanied by reduced Cx43 phosphorylation and plakophilin 2 (PKP2) expression. Moreover, PIASy downregulation remarkably reduced Cx43 SUMOylation, accompanied by increased Cx43 phosphorylation and PKP2 expression after I/R. PIASy downregulation inhibited Cx43 SUMOylation and increased PKP2 expression, thereby improving ventricular arrhythmias in ischemic/reperfused rats heart.