Artificial intelligence (AI) has rapidly emerged as a promising tool for improving autism spectrum disorder (ASD) screening, particularly in regions where access to trained specialists remains limited. Recent advances in machine learning have demonstrated encouraging diagnostic performance through the analysis of facial expressions, speech, eye gaze, and other behavioral markers, offering the potential to expand early diagnosis and reduce disparities in healthcare access. However, existing research has focused predominantly on algorithm development and diagnostic accuracy, while comparatively little attention has been paid to the broader ethical, cultural, and geopolitical implications of AI-assisted autism diagnosis. Drawing upon perspectives from philosophy of medicine and science and technology studies, this paper examines how AI redistributes power through three interconnected shifts: the transfer of diagnostic authority from clinicians to algorithms, the globalization of culturally specific definitions of "normal" behavior through Western-trained datasets, and the emergence of technological dependency on foreign-controlled AI infrastructure. Rather than rejecting AI-assisted diagnosis, this paper argues that equitable implementation requires culturally representative datasets, participatory model development, and greater local ownership of digital health technologies to ensure that AI promotes both diagnostic accessibility and global health equity.

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Various reasons contribute to the development of anxiety disorders in adolescence, and genetics, environment, and their interactions (G×E) are all involved. This systematic review examines recent evidence of genetics, environment and their interaction in the course of development of anxiety disorders during adolescence. Obtained studies from databases and screened them according to PRISMA guidelines. Most of the studies included in this review have frequently mentioned polymorphisms of the serotonin system. The most frequently studied of the serotonin-transporter-linked polymorphic regions was 5-HTTLPR. Based on the above research, allele differences can affect a person's risk of anxiety by altering the mechanism of neurotransmitter transmission and regulation of the stress response system. The Environment may affect the results of anxiety in adolescents. Family-related factors are included in the above, such as parenting style, parents' education, family environment and daily stress. According to research on G×E interactions, genetic risk can be increased or reduced by environmental factors; however, due to differences in the characteristics of the sample studied, anxiety was not measured, and various methods were used, the results of such studies are inconsistent. In short, the above content shows that anxiety disorders in adolescence are the result of multiple factors, and thus, both genetic and environmental factors should be considered when determining the causes of anxiety disorders. The results of this study will provide a reference for improving the present prevention and intervention plan for environmentally vulnerable adolescents.

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Osteoporosis constitutes a significant public health concern among older adults, particularly in rural regions of China. However, data on its prevalence and risk factors in Southern Sichuan are limited. The objective of this study is to assess the prevalence and determinants of osteoporosis among rural seniors aged 60 years and older in Southern Sichuan, and to furnish scientific evidence for community-based preventive strategies. This paper employs a literature review and case analysis approach to examine a cross-sectional study conducted from July to December 2025. The paper finds that the prevalence of osteoporosis among rural elderly in Southern Sichuan is considerably high. Advanced age, female sex, vitamin D deficiency, insufficient outdoor activity, history of fracture, and low health literacy are major risk factors. Community-based osteoporosis screening and health education should be strengthened, and regular outdoor activities together with adequate calcium and vitamin D supplementation should be promoted to reduce the risk of osteoporosis and related fractures.

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The unfolded protein response (UPR) is a homeostatic protective mechanism activated in response to endoplasmic reticulum (ER) stress. However, once co-opted by cancer cells, its function extends far beyond maintaining proteostasis and becomes an important regulator of tumor progression. This review summarizes how the three canonical UPR branches establish a persistent adaptive state under chronic ER stress. It discusses the molecular mechanisms by which UPR signaling maintains proteostasis, reprograms cellular metabolism, alleviates oxidative stress, and coordinates autophagy. Thereby it allows cancer cells to survive in hostile microenvironments. The review further examines how these adaptive programs support tumor metastasis by promoting anoikis resistance, epithelial-mesenchymal plasticity, and tumor dormancy, which also enhances resistance to chemotherapy and immunotherapy. Current evidence suggests that cancer cell survival, metastasis, and therapy resistance are not independent consequences of UPR activation, but interconnected manifestations of a unified stress adaptation strategy driven by the UPR. By clarifying how cancer cells exploit UPR signaling and its underlying mechanisms, this review aims to provide insights into potential specific therapeutic opportunities for cancer.

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