iScience最新文献

Against global net-zero carbon goals and China's "dual carbon" goals, cultural consumption remains trapped in a high-carbon trap (HCT), hindering the sustainable development of environmental and social systems. Using benchmark regression and a mediating effect model, this study explores how new quality productivity (NQP) impacts carbon emissions from cultural consumption. Findings reveal a non-linear "first promoting, then inhibiting" effect of NQP on such emissions. It is worth noting that cultural innovation (CI) serves as a transmission mechanism through which NQP exerts an inverted U-shaped relationship on the HCT in cultural consumption. In addition, energy transition (ET) plays a regulatory role in the inverted U-shaped outcome, which can enhance the inhibitory effect of NQP on carbon emissions from cultural consumption. Overall, this study extends the Environmental Kuznets Curve theory to cultural consumption, offering causal insights and actionable policy implications for the sustainable transformation of environment-social systems.

Microbial optogenetic tools can regulate gene expression with spatial and temporal precision, offering excellent potential for single-cell resolution studies. However, bacterial optogenetic systems have primarily been deployed for population-level experiments. It is not always clear how these tools perform in single cells, where stochastic effects can be substantial. In this study, we focus on optogenetic Cre recombinase and compare the performance of three variants (OptoCre-REDMAP, OptoCre-Vvd, and PA-Cre) for their population-level and single-cell activity. We quantify recombination efficiency, expression variability, and activation dynamics using reporters which produce changes in fluorescence or antibiotic resistance following light-induced Cre activity. We find that optogenetic recombinase performance can be reporter-dependent. Further, single-cell analysis reveals highly heterogeneous activity, with substantial variation in the efficiency and timing of recombinase activity from cell to cell. These findings suggest important criteria for selecting optogenetic recombinases and indicate areas for optimization to improve single-cell capabilities of bacterial optogenetic tools.

Schwann cells (SCs) are glial cells of the peripheral nervous system with functional plasticity in physio-pathological conditions, such as injury and oncotransformation. Interestingly, human SCs seem to develop, mature, and respond differently to other species to environmental challenges. Recently, concerns have been raised about the expansion of environmental electromagnetic fields (EMFs) and the increasing incidence of vestibular schwannoma (VS). We previously demonstrated that SCs respond to EMF by acquiring a state prone to oncotransformation. However, the biodependence of such transformation on the species (rodents versus humans) deserves clarification. Here, we obtained and characterized human SCs, showing that EMF affects proliferation, migration, and transcriptomic profile. The expression of motility proteins increased, while that of cell-to-cell adhesion proteins decreased. The functional clustering of genes differentially expressed matched those involved in hearing loss. In summary, we provide insights into the effects of chronic EMF on human SCs, highlighting its potential role in VS onset.

The skin is a highly innervated and vascularized organ that acts as a frontline sensor of environmental and internal physiological cues. While psychological stress and prolonged ultraviolet (UV) exposure aggravate inflammatory skin conditions, the underlying mechanisms remain elusive. Here, we identify a neurovascular mechanism whereby stress-induced sympathetic hyperactivation compromises vascular barrier integrity in the skin. Using surgical or chemical denervation, optogenetics, intravital imaging, and genetic models, we show that both acute psychological stress and high-dose UV exposure activate the skin sympathetic nervous system, triggering norepinephrine release and α2B-adrenergic receptor signaling in dermal endothelial cells. This pathway leads to RhoA/ROCK-mediated Claudin-5 disruption, resulting in increased vascular permeability and heightened immune cell infiltration. Pharmacological or genetic inhibition of this axis restores vascular stability and attenuates inflammation. These findings reveal that skin vasculature decodes sympathetic tone, highlighting potential therapies for stress-aggravated skin disorders.

Sonodynamic therapy (SDT) for deep-seated tumors is limited by tumor microenvironment (TME) barriers. We developed a hyaluronic acid (HA)-modified mesoporous calcium carbonate nanoplatform (HA/CaCO₃@Ce6) to synergistically enhance calcium overload and SDT. The CD44-targeted nanoplatform demonstrated pH-responsive degradation in acidic TME, resulting in the release of Ca²⁺ and chlorin e6 (Ce6). The released Ca²⁺ induced mitochondrial calcium overload, causing 71% collapse in membrane potential and 1.6-fold increase in reactive oxygen species (ROS) generation, establishing a "Ca²⁺-ROS positive feedback loop." This synergy triggered robust immunogenic cell death (ICD), enhancing CRT exposure by 94.2%, HMGB1 release by 46.2%, and ATP decrease by 74.5%. In vivo, it achieved 90.9% tumor inhibition and 80% 60-day survival rate, alleviated tumor hypoxia, and inhibited tumor proliferation and angiogenesis. This "ion-interference SDT" paradigm overcomes the limitations of SDT through self-amplified ROS cycle and provides an effective strategy for treating deep-seated solid tumor with significant clinical translation potential.

To investigate ethnic differences inprogression from prediabetes to diabetes in a multi-ethnic community, and develop prediction models for diabetes risk and glycemic progression. This 4.7-year retrospective cohort included 4,726 non-diabetic Han, Yi, and Dai individuals. Cox regression was used to analyze the cumulative incidence of diabetes. Two prediction models were developed and validated: a diabetes risk model and GlycoStep, a model for glycemic progression. Prediabetes was significantly associated with diabetes development (HR = 2.25). Over 4.7 years, the cumulative diabetes incidence was 12.7% in the prediabetes group versus 5.5% in normoglycemic individuals. The Yi had the highest incidence, followed by Han and Dai. The diabetes risk model achieved a C-index of 0.76 and AUCs of 0.65-0.80 over 2-4 years, demonstrating effective predictive performance. Similarly, the GlycoStep model exhibited strong predictive ability (C-index: 0.66; AUC range: 0.68-0.77), with ethnic-specific variations. These findings highlight ethnic disparities in diabetes progression and support individualized prevention strategies in multi-ethnic communities.

Atherosclerosis (AS), a chronic inflammatory disorder initiated by vascular endothelial dysfunction (ED), is prominently triggered by hemodynamic low-shear stress (LSS). Interferon regulatory factor 6 (IRF6) is a transcription factor that regulates the inflammatory response following injury. In this work, the LSS-induced AS model was induced by the partial ligation of the left carotid artery in high-fat diet-fed ApoE^-/- mice. After four weeks of feeding, AS mice exhibited higher IRF6 expression and more severe lesions than sham mice. IRF6 suppression alleviated ED, inflammatory response, and oxidative stress in LSS-induced AS mice. In LSS-treated human aortic endothelial cells (HAECs), IRF6 was also highly expressed. Inhibition of IRF6 reduced the expression of pro-inflammatory adhesion molecules and the adhesion of THP-1 cells to HAECs. Mechanistically, IRF6 transcriptionally upregulated NDRG1. NDRG1 upregulation reversed the beneficial effect of IRF6 knockdown. Overall, IRF6 induces ED through the transcriptional activation of NDRG1, aggravating LSS-mediated AS progression.

Urban management faces unprecedented challenges in addressing uncertainty, maintaining ecological balance, and safeguarding social welfare. Despite artificial intelligence (AI) providing opportunities while also posing risks, empirical evidence of its impact on urban resilience remains limited. Using panel data from 266 prefecture-level cities in China for the period between 2011 and 2022, this study examined the impact of AI development on urban resilience and elucidated the underlying mechanisms based on the technology-organization-environment framework. The key findings are as follows: AI development exerts an inverted U-shaped influence on urban resilience; the partial mediating roles of fiscal decentralization and financial resources are identified; governmental response exhibits a moderating effect on the relationship and moderates the mediating effect of fiscal decentralization; and economic development moderates the effect of AI on urban resilience, operating partially through financial resources. Several policy recommendations are provided to support cities in leveraging AI development to strengthen urban resilience.

Attentional bias modification training is commonly employed to regulate attentional bias and alleviate symptoms of mental disorders, but its efficacy is constrained and inconsistent. To address this challenge, we introduced an attention switch training method grounded in the rhythmic theory of attention. A total of 135 university students with negative attentional bias were randomly assigned to one of four groups: with/without rhythm-based training × with/without probability-based training. Each participant completed a single training session and underwent the Self-Assessment of Valence Task and the Dot Probe Task (DPT) before and after training. The results indicated that theta rhythm training led to a greater reduction in negative attentional bias, mainly by enhancing the disengagement of attention from negative stimuli. Regression analysis revealed an inverse relationship between initial attentional scores and training effects, with the rhythm-based training showing the strongest correlation. Overall, the rhythm-based training offers a more effective framework for modifying attentional bias with a mechanism of attention shift based on the theta trough.

Phosphorylation plays a critical role in regulating immune responses in invertebrates. In Penaeus vannamei, hemocyanin, a multifunctional immune protein, is cleaved to produce antimicrobial peptides (AMPs) essential for pathogen defense. This study identifies Ser548 phosphorylation of the hemocyanin small subunit (PvHMCs) as a key regulator of trypsin-mediated hemocyanin degradation and antimicrobial peptides production. Dephosphorylation of Ser548, controlled by PvCK2α kinase and PvPP2AC phosphatase, enhances cleavage, generating peptides with strong antibacterial activity against Vibrio parahaemolyticus and Streptococcus iniae. Phosphorylation inhibits this process, reducing peptide production and immune efficacy. In vivo, Ser548 dephosphorylation improves bacterial clearance and enhances shrimp survival. These findings reveal a critical molecular mechanism underlying shrimp immunity and suggest targeting hemocyanin phosphorylation to boost disease resistance in aquaculture.