Traumatic brain injury (TBI) induces neuroimmune activation and metabolic reprogramming in microglia, but the transcriptional regulators underlying these responses remain unclear. This study aimed to integrate single-cell and bulk transcriptomic datasets to identify microglia-associated regulatory genes and characterize their potential roles in post-TBI neuroinflammatory and immunometabolic dysregulation.

We integrated single-cell RNA sequencing data (GSE101901) with a bulk training dataset (GSE58485) and an independent bulk validation dataset (GSE242025) from murine TBI models. hdWGCNA, differential expression, pseudotime, CIBERSORT, and in silico transcription factor binding-site analyses were performed to identify and characterize candidate genes. Key-gene expression was additionally validated by RT-qPCR in male C57BL/6 mice assigned to Sham and TBI groups (n = 5 per group). The Drug Gene Interaction Database was used for exploratory drug-gene prediction.

Single-cell profiling suggested descriptive shifts in the proportions of microglia, astrocytes, and neurons after TBI. hdWGCNA identified 90 microglia-associated genes, 43 of which overlapped with nominally differentially expressed genes; 89 genes met the Benjamini–Hochberg-adjusted P < 0.05 threshold in the bulk analysis. Cross-dataset validation identified increased Ccl4 and Lgals3 expression and decreased Egr1 expression. Motif scanning identified four predicted EGR1 motif occurrences in the Ccl4 promoter and six occurrences at three unique locations in the Lgals3 promoter. RT-qPCR in TBI and Sham mice (n = 5 per group) supported the same directional expression changes in Ccl4, Lgals3, and Egr1.

A candidate Ccl4/Lgals3/Egr1 expression pattern characterized by Ccl4 and Lgals3 upregulation and Egr1 downregulation was associated with post-TBI neuroinflammatory and immunometabolic changes. Further mechanistic validation is required.

Endovascular embolization is a cornerstone treatment for intracranial aneurysms, and transfemoral access (TFA) has traditionally been the default vascular route. Transradial access (TRA) is increasingly used in neurointervention because it may reduce clinically important access-site complications, improve postprocedural comfort, and facilitate earlier ambulation. This narrative review aims to summarize direct and indirect evidence comparing TRA and TFA for intracranial aneurysm embolization, with attention to technical feasibility, access conversion, puncture-site complications, neurological events, radiation exposure, procedure duration, recovery, and cost considerations. Direct comparative evidence specific to aneurysm embolization remains limited and is mainly observational; some supporting data come from diagnostic cerebral angiography, mixed therapeutic neurointervention, and cardiovascular access literature. Available data suggest that TRA may be a safe and feasible option for selected patients when performed by experienced operators, particularly when radial anatomy is favorable and the intended device strategy is compatible with upper-extremity access. TFA remains essential for complex anatomy, large-bore device requirements, or insufficient TRA expertise. Access selection should therefore be individualized rather than based on a presumption of universal superiority. Well-designed multicenter studies are needed to define aneurysm-specific outcomes, long-term angiographic durability, patient-reported outcomes, and cost-effectiveness.

The widespread assumption that “natural” equals “safe” has been repeatedly challenged by adverse events associated with medicinal plant-derived products. Unlike synthetic pharmaceuticals, these natural products present distinct safety concerns because of their compositional complexity, inherent variability, and batch-to-batch inconsistency. Consequently, a one-size-fits-all approach to toxicological assessment is insufficient. In this narrative review, we propose a pragmatic “classify-then-evaluate” framework that stratifies natural products into three operational categories according to compositional complexity and degree of chemical characterization—TCM compound formulae, active fractions/extracts, and purified single compounds. This framework enables safety evaluations to be tailored to product complexity by integrating conventional toxicological assays with emerging new approach methodologies. By linking chemical characterization, hazard identification, quality control, and risk assessment within a tiered system, this framework bridges the gap between evidence generation and regulatory decision-making, offering a scientifically grounded and proportionate pathway for evaluating the safety of natural products used in integrative medicine, with a primary focus on herbal and TCM-related products. The review does not aim to provide a comprehensive systematic evidence map; further validation of the proposed framework is required

Colorectal cancer is a major cause of cancer morbidity and mortality worldwide, including in China. Screening can facilitate earlier detection and reduce disease burden, while primary healthcare institutions are central to population outreach, risk assessment, referral, and follow-up. However, resource constraints, limited public awareness, low screening adherence, and fragmented coordination continue to hinder implementation in community and rural settings. This mini review summarizes the epidemiological and health-economic rationale for colorectal cancer screening in primary healthcare and discusses organizational models, risk-stratified screening and referral, workforce training, quality control, data management, and information sharing. Available evidence supports coordinated pathways that link noninvasive initial screening to timely colonoscopy and follow-up, supported by clear governance, trained personnel, and traceable data systems. The ongoing Yazhou District program is included briefly as a descriptive example of how these components may be organized in practice. Future research should evaluate uptake, positivity, colonoscopy completion, lesion detection, adverse events, costs, and longer-term outcomes in diverse primary-care settings.

Hepatitis B virus (HBV) reactivation is a well-recognized complication in patients with lymphoma receiving immunosuppressive therapy, particularly rituximab-containing regimens. We describe a 58-year-old man with diffuse large B-cell lymphoma and an atypical baseline HBV serological profile: hepatitis B surface antibody (anti-HBs) positivity (102.00 U/L), antibody to hepatitis B core antigen negativity, a low-level hepatitis B surface antigen (HBsAg) result (0.35 COI, reported as negative by the local laboratory), and undetectable HBV DNA. Thirteen days after initiation of the fourth cycle of modified R-CHOP (rituximab, cyclophosphamide, pirarubicin, vinorelbine and dexamethasone) chemoimmunotherapy, the anti-HBs titer had decreased to 1.31 S/CO, the HBsAg level to 0.02 S/CO, and HBV DNA was not reassessed until reactivation. Approximately 16 weeks after treatment completion, the patient developed fatigue, anorexia, and jaundice. HBsAg increased from 28.66 S/CO to 8048.30 IU/mL, hepatitis B e antigen became positive, and HBV DNA increased to 1.94 × 109 IU/mL. Despite treatment with tenofovir alafenamide fumarate and plasma exchange, the patient died of refractory liver failure and hepatic encephalopathy. These findings suggest that atypical serological profiles may not reliably indicate a low risk of severe HBV reactivation during intensive immunosuppressive therapy. Comprehensive pretreatment risk assessment and long-term monitoring of anti-HBs titers, HBsAg, and HBV DNA during and after therapy may facilitate earlier detection and intervention.