Purpose: The integration of social media into all areas of society has become a typical phenomenon of the Internet era. This study’s core objective is to dissect the relationship between social media, self-efficacy and loneliness, especially emphasizing the mediating function of social support. Patients and Methods: The research data is derived from the pooled cross-sectional data combined from the four-period data of the China Family Panel Studies (CFPS). The study employs Ordinary Least Squares (OLS) regression as the basic research method, and utilizes Instrumental Variables (IV) and other methods to conduct robustness checks. Results: Social media usage frequency (SMUF) enhances self-efficacy and loneliness through social support. Social support promotes self-efficacy and alleviates users’ loneliness. In self-efficacy, social support plays a fully mediating role. Moreover, education (human capital) has a significant moderating effect. There are noticeable differences in the response of different characteristics groups to SMUF. Conclusion: This study reveals how social media impacts self-efficacy and loneliness through social support. Based on the research results, avoiding prolonged usage of social media and improving digital literacy are the crucial means to exert the positive benefits of social media.

Objectives: The aim of this study was to explore the mechanism between public services and residents’ health, focusing on the role of spatial geographical factors.Methods: Leveraging a comprehensive panel dataset encompassing 30 mainland Chinese provinces from 2007 to 2019, this study engineered a spatial Durbin model furnished with dual fixed effects through the application of the Lagrange multiplier, Hausman, and likelihood ratio tests. The primary objective was to delve into the repercussions of varying public service levels on residents’ health outcomes.Results: The empirical findings reveal a palpable spatial autocorrelation between residents’ health outcomes and the public services levels dispensed across Chinese provinces. Intriguingly, an elevation in the public service level in a given province not only ameliorates its residents’ health outcomes but also triggers a spatial spillover effect, thereby positively influencing residents’ health in neighboring provinces. The rigorous endogeneity and robustness checks affirm the reliability of the principal outcomes.Conclusion: Due to the increase in social uncertainty, all regions should break free of the administrative monopoly, enhance regional integration and development, and improve residents’ health status by clustering public service supply.

In the current tide of technological revolution and industrial transformation, digitalization and greening have surfaced as two prominent trends, serving as the inherent requisites and impelling forces of new productive forces. Augmenting carbon emission efficiency is a crucial pathway for attaining green development. Digital inclusive finance, as an innovative financial paradigm, is a significant determinant influencing carbon emission efficiency and the progression of green development. By harnessing panel data from 108 cities within the Yangtze River Economic Belt spanning from 2011 to 2021, this study deploys the super-efficiency SBM model to gauge carbon emission efficiency. Additionally, it employs fixed effects and mediating mechanism models to empirically scrutinize the impact of digital inclusive finance on carbon emission efficiency within urban agglomerations in the Yangtze River Economic Belt. The study further probes its spatial effects through a spatial Durbin model. The research findings disclose that digital inclusive finance can substantially augment carbon emission efficiency in regional cities along the Yangtze River Economic Belt, manifesting notable regional correlations. This enhancement is accomplished by propelling industrial structure upgrades and augmenting scientific and technological capabilities. To enhance carbon emission efficiency in the Yangtze River Economic Belt, efforts should be centered around advancing digital inclusive finance, expediting industrial structural transformation, and fortifying scientific and technological development.

Background: Triggering receptor expressed on myeloid cells 2 (TREM2) is a pivotal lipid‐sensing receptor that governs the functional plasticity and metabolic fitness of mononuclear phagocytes, including microglia, osteoclasts, dendritic cells and tissue‐resident macrophages. While originally identified as a genetic risk factor for Alzheimer's disease (AD), TREM2 functions as a context‐dependent immunometabolic checkpoint rather than a uniform phenotypic driver, exerting divergent biological outputs dictated by distinct tissue microenvironments and ligand repertoires. Summary of key contents: This review provides a comprehensive synthesis of TREM2 immunobiology, detailing how ligand engagement—including cell‐surface phospholipids and apolipoprotein E (ApoE)—activates the DAP12/DAP10–SYK–PI3K–mTOR signalling axis. This coordinated intracellular cascade instructively drives myeloid adaptation towards metabolically competent disease‐associated microglia (DAM) and lipid‐associated macrophage (LAM) states, sustaining bioenergetics and debris clearance under pathological stress. Across neurodegenerative proteinopathies and acute cerebral ischemia, TREM2 signalling is predominantly neuroprotective by promoting aggregate compaction and mitigating secondary excitotoxicity, although chronic dysregulated activation may drive stage‐dependent neuroinflammation. In peripheral inflammatory pathologies such as rheumatoid arthritis and sepsis, TREM2 fine‐tunes macrophage efferocytosis and systemic metabolic thresholds. In oncology, TREM2 displays a complex, microenvironment‐dependent divergence: in central nervous system malignancies such as glioblastoma (GBM), TREM2 exerts controversial, stage‐dependent effects, spanning microglial tumour containment in early stages versus pro‐tumoural myelin recycling and immunosuppression by monocyte‐derived macrophages in post‐treatment recurrence; conversely, in peripheral solid tumours, monocyte‐derived TREM2+ tumour‐associated macrophages (TAMs) predominantly orchestrate an immunosuppressive, nutrient‐deprived niche that impairs cytotoxic T‐cell function. Furthermore, we synthesise emerging paradigms along the bidirectional microbiome–gut–brain–tumour axis, elucidating how commensal and intra‐tumoural microbial cues dynamically calibrate myeloid signalling tone and therapeutic susceptibility. Conclusion: We address translation bottlenecks—including blood–brain barrier (BBB) shuttles, human trial scarcity and soluble TREM2 (sTREM2) biomarker harmonisation—outlining a biomarker‐guided, context‐tailored precision therapeutic framework for targeting the TREM2 axis.