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.

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

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.

Metabolic dysfunction–associated steatotic liver disease (MASLD) and alcohol–associated liver disease (ALD) are leading causes of chronic liver injury with overlapping clinical and histological presentations. This study evaluated a composite histologic pattern, termed the Alcohol Liver Pathology Signature (ALPS), for potential use in the differential diagnosis of ALD and MASLD and to explore potential clinical and demographic correlates.

In this retrospective diagnostic-accuracy study, we reviewed 292 liver biopsies performed between 2021 and 2023. ALPS comprised five histologic features: ductular reaction, bile stasis, neutrophilic satellitosis, portal inflammation, and advanced fibrosis (stage 3–4). Cases were categorized as absent (0–1 features), partial (2–3 features), or full (4–5 features). ALPS performance was then further evaluated in an independent temporal validation cohort of de-identified, mixed, and blindly reviewed liver biopsies collected between 2024 and 2025.

MASLD was the most common diagnosis (25.3%), whereas ALD accounted for 4.8%. Full ALPS was present in 92.8% of clinically diagnosed ALD cases. In MASLD, individual ALPS features were common, but only 20.3% showed full ALPS, corresponding to 79.7% specificity for distinguishing clinically diagnosed ALD from MASLD. The independent temporal validation cohort showed findings consistent with those of the original cohort. Finally, within MASLD, full ALPS was more frequent in African American than non-African American patients (29.2% vs. 3.8%).

ALPS may serve as a histologic prompt for further assessment of potential alcohol exposure but should not be considered etiologically specific. Prospective validation incorporating objective measures of alcohol exposure is warranted.

Watertight-intent dural reconstruction may reduce incisional cerebrospinal fluid (CSF) leakage after decompressive craniectomy but may prolong surgery. We aimed to evaluate whether watertight-intent reconstruction, compared with non-watertight management, was associated with direct postoperative incisional CSF leakage and operative time.

Five databases were searched through August 1, 2026. Comparative studies with explicit watertight or sealing-intent reconstruction and non-watertight comparators were included. The primary outcome was direct incisional CSF leakage; secondary outcomes included operative time, wound or surgical-site infection, hydrocephalus, mortality, and functional outcomes. Binary outcomes were expressed as risk ratios (RRs), and continuous outcomes as mean differences. Random-effects meta-analysis used restricted maximum likelihood estimation with Wald 95% confidence intervals (CIs); randomized and observational studies were examined as subgroups, with Hartung–Knapp sensitivity analyses. Certainty of evidence was assessed using the Grading of Recommendations Assessment, Development and Evaluation framework.

Twelve studies were included; nine (1,314 participants) reported direct incisional CSF leakage. Watertight-intent reconstruction was associated with fewer reported leaks (RR, 0.54; Wald 95% CI, 0.34–0.86; I² = 23.3%), although the prediction interval included the null value (0.24–1.20). The randomized subgroup was imprecise (RR, 0.75; 95% CI, 0.32–1.73), whereas the observational subgroup favored reconstruction (RR, 0.43; 95% CI, 0.20–0.90); its Hartung–Knapp interval (0.14–1.32) crossed 1. Infection and hydrocephalus estimates were imprecise; mortality and function were not pooled. Reconstruction was associated with longer operative time (mean difference, 39.85 minutes; 95% CI, 25.14–54.56; I² = 97.4%). Certainty was very low for all key outcomes.

Watertight-intent reconstruction is associated with fewer reported incisional CSF leaks and longer operations, although certainty is very low. Limited study and event numbers, imprecise design subgroups, and multicomponent techniques preclude causal or universal treatment conclusions. Effects on infection, hydrocephalus, mortality, and function remain uncertain.

Hepatocellular carcinoma (HCC) exhibits profound metabolic reprogramming, with enhanced aerobic glycolysis and excess lactate production as defining features. Lactate, once regarded simply as a metabolic byproduct, is now recognized as a powerful epigenetic driver through lysine lactylation, while tumor cells co-opt autophagy to endure metabolic stress. Although traditionally investigated as separate hallmarks of cancer, growing evidence points to their functional intersection. Here, we propose the concept of a coordinated “lactylation-autophagy axis” and clarify its role in remodeling the tumor immune microenvironment. Within this integrated metabolic-epigenetic-proteostatic network, lactate-induced histone lactylation, such as H3K18la, exerts transcriptional control over tumor-associated macrophages, shifting them toward an immunosuppressive M2-like state. Excess extracellular lactate and robust autophagic adaptation cooperate to impair the effector functions of CD8+ T cells and natural killer cells, while providing regulatory T cells with metabolic advantages. We further explore the bidirectional crosstalk within this axis: lactate modulates autophagic flux, potentially through mTOR signaling and non-histone lactylation of autophagy-related proteins (e.g., VPS34, TFEB), whereas autophagy in turn regulates intracellular metabolite pools and lactylation substrates. Notably, several nodes, particularly non-histone lactylation of VPS34, TFEB, and mTOR (K921), have been demonstrated mainly in non-HCC systems; we therefore grade each mechanism as confirmed in HCC, extrapolated from other systems, or hypothetical. This proposed self-reinforcing axis may sustain tumor plasticity, contribute to immune evasion and immunotherapy resistance, and we discuss rational combinatorial strategies—combined targeting of lactate metabolism, lactylation machinery, and autophagic pathways—to sensitize advanced HCC to immune checkpoint blockade.