Cyberbullying among adolescents often takes place in front of an online audience, yet many bystanders remain passive. Evidence on factors associated with intervention is dispersed across psychological, relational, contextual, and platform-related areas.

Immune genetic variation and lifestyle factors jointly influence cancer susceptibility, but their interactions in cancer development remain unclear. We evaluated the independent and joint effects of lifestyle profiles and classical HLA alleles on overall and site-specific cancer risks using sex-stratified analyses.

Mitochondrial Ca[2+] homeostasis is a critical interface connecting ovarian cell signaling, energy metabolism, redox balance, and reproductive competence. Transient Ca[2+] uptake into the mitochondrial matrix activates Ca[2+]-sensitive dehydrogenases, enhances reducing-equivalent generation, and supports oxidative phosphorylation. By contrast, sustained Ca[2+] accumulation promotes reactive oxygen species production, membrane-potential collapse, mitochondrial permeability transition, and cell death. The identification of the mitochondrial calcium uniporter together with its regulators MICU1, MICU2, and EMRE, has established a molecular framework for mitochondrial Ca[2+] influx. NCLX and its interacting protein TMEM65 contribute to Ca[2+] efflux and determine recovery after individual Ca[2+] transients. In ovarian cells and oocytes, endoplasmic reticulum (endoplasmic reticulum)-mitochondria contact sites, including the IP3R1-GRP75-VDAC1 axis, couple cytosolic Ca[2+] signals to mitochondrial metabolism. Evidence from mouse, porcine, avian, zebrafish, Xenopus, and sea-urchin models implicates mitochondrial Ca[2+] in follicular-cell survival, oocyte meiotic maturation, fertilization-associated Ca[2+] oscillations, the oocyte-to-embryo transition, and early embryonic development. Obesity, aging, cryopreservation, heavy metals, environmental chemicals, and oxidative stress can disturb this system. However, mitochondrial Ca[2+] dysregulation is not always readily separable from broader mitochondrial or ER dysfunction. Major limitations of the current literature include reliance on non-selective pharmacological agents, incomplete calibration of organelle-targeted indicators, insufficient temporal resolution, interspecies differences, and limited direct evidence from human oocytes. Future studies should integrate cell-type-specific genetic perturbation, quantitative multi-organelle Ca[2+] imaging, mitochondrial bioenergetics, and long-term developmental assessment. Mitochondrial Ca[2+] is a promising mechanistic node and candidate biomarker, but it is not yet a validated clinical target in reproductive medicine.

Climate risk shocks to the global supply chain are becoming more severe, and the pharmaceutical industry is especially vulnerable, given the high stakes of patient safety, cold-chain constraints, geographic concentration of active pharmaceutical ingredients, and stringency of quality regulation. Using panel data on pharmaceutical manufacturers listed in the A-share from 2003 to 2024, we construct a climate risk perception indicator based on the textual analysis of annual reports and examine its impact on the supply chain resilience of firms and the mechanisms involved. Our findings show that the heightened climate risk perception significantly enhances supply chain resilience. This relationship is robust to alternative dependent and independent variables, alternative specifications of fixed effects, and different trimming ranges. Three mechanisms drive the effects: (i) promoting green innovation, (ii) deepening supplier relationships, and (iii) diversifying customer concentration. The heterogeneity analyses suggest that the effects are stronger for state-owned enterprises, smaller firms, and firms with higher managerial risk aversion. This study connects climate risk perception and supply chain resilience in a regulated pharma context, offering new theory and empirical evidence for resilience in relationship-driven supply chains.

This study examines how Automatic Speech Recognition (ASR) technology can enhance college English speaking instruction by analyzing its interaction with metacognitive strategies and learner differences. Using questionnaire surveys, factor analysis, and structural equation modeling, we assess how ASR-generated feedback quality, structured reflection tasks, and usage frequency influence feedback internalization, reflective learning, and motivation. The results show that accurate error correction and well-designed reflection tasks significantly improve feedback processing and reflective behavior, while frequent ASR use primarily boosts reflection rather than motivation. Interestingly, ASR accuracy enhances intrinsic motivation but does not directly drive reflection. Language proficiency emerges as a key moderator, with more proficient learners internalizing feedback more effectively and achieving greater speaking gains. The study contributes to second language acquisition theory by integrating metacognitive strategies with ASR-assisted learning. It provides empirical support for intelligent teaching systems and practical guidance for improving oral English instruction, intercultural communication training, and personalized learning. By bridging technology and pedagogy, this research advances active learning methodologies, enhances speaking proficiency, and strengthens the global competitiveness of higher education.

Chlamydia is an obligate intracellular bacterial pathogen responsible for sexually transmitted infections and blindness worldwide. In our search for antichlamydial agents from natural sources, we identified pyocyanin, a phenazine derivative from Pseudomonas aeruginosa. Previous studies showed that pyocyanin disables elementary body (EB) infectivity at low concentrations and inhibits intracellular growth at higher concentrations. In the present study, we show that its antichlamydial activity is primarily attributed to the intracellular developmental stage. Complete inhibition of detectable infectious progeny was achieved at 16 μM at the standard 36 hpi endpoint, while its effect on the infection stage reached only approximately 60% inhibition. Two independent delayed treatment assays revealed that pyocyanin reduces the infectivity of newly formed EBs without reducing their number. Furthermore, pyocyanin delays rather than arrests the chlamydial developmental cycle, and its inhibitory effect is reversible, requiring sustained drug exposure for optimal efficacy. These findings position pyocyanin among a growing class of antichlamydial agents that target distinct steps of the pathogen's developmental cycle and support its potential as a chemical probe for chlamydial biology and a lead compound for drug development.