Cervical cancer is a major malignancy that threatens women’s health, and early screening is a core strategy for reducing its incidence and mortality. Multimodal fusion artificial intelligence (AI) pathological diagnosis models integrate multidimensional data—including cytological images, colposcopic images, whole-slide histopathological images, clinical data, and molecular testing results—and may enhance the detection sensitivity, grading accuracy, and screening efficiency for early cervical cancer and precancerous lesions. However, traditional cervical cancer screening methods face limitations such as high subjectivity, reliance on single-source information, relatively low efficiency, and insufficient primary care resources. Furthermore, existing reviews mostly focus on single-modal AI models or specific technical aspects, lacking a comprehensive analysis of the full technical framework and clinical translation pathways of multimodal fusion models. This review aims to comprehensively present the development and application of multimodal fusion AI models in pathological diagnosis for early cervical cancer screening. Specifically, it comprehensively details the technical architecture, data modalities, and fusion strategies—including deep learning, attention mechanisms, and cross-modal alignment techniques—that enable the complementary representation of morphological, clinical, and molecular information. Additionally, the review integrates recent advances in clinical applications and evaluates current translational challenges, providing insights into clinical validation pathways to bridge technological innovation and practical healthcare delivery. In conclusion, with further technological refinement and clinical validation, multimodal fusion AI may become a useful tool for improving the precision and efficiency of cervical cancer screening and prevention, and may inform the standardized application and translational research of AI technology in this field.

In contemporary practice, elevated 24-hour urinary copper excretion (24-h UCE) often triggers referral for suspected Wilson disease (WD). In this hypercupriuric referral setting, interpretation of 24-h UCE may be distorted by spectrum effects. In this study, we aimed to compare conventional copper biomarkers in hypercupriuric referrals and evaluate whether a Leipzig-aligned ceruloplasmin (Cp) framework could provide a clinically useful triage approach.

We retrospectively studied consecutive, untreated patients evaluated for suspected WD with hypercupriuria between February 2017 and February 2025. The final diagnosis was established using a prespecified Leipzig-based algorithm, with ATP7B testing when indicated. Diagnostic performance of Cp and 24-h UCE was compared. A prespecified Cp three-zone framework was evaluated using <0.10 g/L, 0.10–0.20 g/L, and >0.20 g/L as high-probability, indeterminate, and low-probability zones, respectively.

Among 541 untreated hypercupriuric patients, 65 had WD and 476 had adjudicated non-WD liver disease. Cp outperformed 24-h UCE for diagnosing WD (AUROC, 0.988 vs. 0.762). The optimal Cp cutoff was 0.15 g/L, with 90.8% sensitivity and 97.7% specificity. Cp < 0.10 g/L defined a high-probability zone with 98.0% WD prevalence, whereas Cp > 0.20 g/L defined a low-probability zone with 0.5% WD prevalence. Among non-WD controls, higher urinary copper was independently associated with higher bilirubin, prolonged international normalized ratio, and lower albumin.

In hypercupriuric referrals for suspected WD, Cp retained strong diagnostic performance and outperformed 24-h UCE. A Leipzig-aligned Cp three-zone framework may support probability-based triage in contemporary referral practice.

Hepatitis B virus (HBV) genotype C is common in East Asia and is associated with poor outcomes, particularly liver cirrhosis and hepatocellular carcinoma (HCC). Clinically, genotype C infection is generally associated with persistent viral replication, later HBeAg seroconversion, more active hepatic inflammation, and an increased risk of HCC. Current evidence suggests that these features are driven by several key molecular events, including the A1762T/G1764A double mutation in the basal core promoter, the G1896A mutation in the precore region, abnormal hepatitis B virus X protein function, and viral integration. Together, these changes may reshape viral transcription, antigen expression, host immune interactions, and oncogenic signaling, thereby contributing to disease progression and hepatocarcinogenesis. Other factors, such as epigenetic changes, dysregulated DNA damage responses, impaired tumor protein p53 function, and disrupted autophagy, may also be involved, although their exact roles remain unclear. Notably, even after effective viral suppression with potent nucleos(t)ide analogs, patients with genotype C may still have a relatively high residual risk of HCC. This review summarizes the molecular virological features, pathogenic mechanisms, immune dysregulation, and clinical significance of HBV genotype C, and discusses the potential value of genotype information in risk stratification, long-term surveillance, and clinical assessment of chronic hepatitis B.

Apatinib has been shown to be efficacious in the treatment of gallbladder cancer. However, the underlying mechanisms remain unclear. This study aimed to explore pathways related to the antitumor effects of apatinib at the cellular level in gallbladder cancer.

NOZ and GBC-SD gallbladder cancer cells were treated with apatinib at concentrations of 0 μM, 10 μM, or 20 μM. The effect of apatinib on the proliferation of these cells was assessed using MTT and colony formation assays, and the effects of apatinib on cell cycle progression and DNA synthesis were evaluated using flow cytometry. Clinical cancer tissue samples, along with paired adjacent normal tissue samples, were obtained from 10 patients with gallbladder cancer. Immunohistochemistry, western blotting, and quantitative real-time polymerase chain reaction analyses were conducted to elucidate molecular changes induced by apatinib treatment.

Treatment with 20 μM apatinib significantly inhibited the expression of phosphorylated (p)-vascular endothelial growth factor receptor 2 (VEGFR2), p-AKT, and histone deacetylase 1 (HDAC1). Additionally, apatinib treatment led to upregulated expression of p-cyclin-dependent kinase 1, p21, and Bax, and downregulated expression of cell division cycle 25B, B-cell lymphoma 2, Snail, and Slug. Apatinib decelerated DNA replication and induced cell cycle arrest at the G2/M phase, consequently suppressing the proliferation of gallbladder cancer cells.

Apatinib inhibits the proliferation of gallbladder cancer cells, and the mechanism involves VEGFR2/AKT, HDAC1, and downstream genes. These findings provide a basis for further investigation into the molecular mechanisms underlying the inhibitory effect of apatinib in gallbladder cancer.

Observational studies indicate frequent associations between systemic lupus erythematosus (SLE) and various hematologic disorders, yet causal inferences are limited by confounding and reverse causality. We therefore applied a bidirectional Mendelian randomization (MR) design to assess potential genetic causal associations of SLE with specific hematologic conditions.

We used European-ancestry GWAS summary statistics for SLE (5,201 cases, 9,066 controls) and five hematologic outcomes (vitamin B12 deficiency anemia (B12DA), myelodysplastic syndrome (MDS), immune thrombocytopenia (ITP), agranulocytosis (AGC), iron deficiency anemia (IDA)) from FinnGen. The primary analysis used inverse-variance weighting, supplemented by MR-Egger and weighted median methods, with comprehensive sensitivity analyses, including heterogeneity tests, pleiotropy assessment, and leave-one-out analysis.

Bidirectional MR analysis revealed that genetically predicted SLE increased the risk of B12DA (odds ratio (OR) = 1.08, P < 0.001), and genetically predicted B12DA was associated with an increased risk of SLE (OR = 2.22, P = 1.6 × 10−29). The MDS → SLE association was nominally significant (P = 0.023) but did not survive Bonferroni correction (P < 0.005) and was inconsistent across MR methods. No significant genetic associations were found between SLE and ITP, AGC, or IDA in either direction (all P > 0.005).

This bidirectional MR study provides genetic evidence that SLE increases the risk of B12DA, whereas the reverse direction (B12DA → SLE) should be interpreted cautiously because it was based on only five instruments and was not supported by the Steiger directionality test. No robust genetic associations were found for ITP, AGC, IDA, or MDS. Clinically, monitoring B12DA in SLE patients may be warranted, although screening recommendations await prospective validation.

Bioactive peptides encrypted within food proteins and released by enzymatic hydrolysis or gastrointestinal digestion represent potential functional ingredients. Amaranth is an underutilized pseudocereal with a balanced amino acid profile and a protein composition that may yield peptides with diverse biological activities. However, translation of amaranth-derived peptides remains limited by low or uncertain bioavailability, variable yields, extraction and purification challenges, incomplete sequence identification, insufficient genotype screening, limited understanding of structure-activity relationships, and scarce in vivo and clinical validation. This review summarizes current evidence on the production, characterization, and pharmacological potential of amaranth-derived bioactive peptides. Enzymatic hydrolysis, fermentation, gastrointestinal digestion, and protein engineering have generated peptide fractions or sequences with antioxidant, antimicrobial, angiotensin-converting enzyme-inhibitory, dipeptidyl peptidase IV-inhibitory, hypocholesterolemic, anti-inflammatory, antithrombotic, and anticancer activities, primarily in in silico, biochemical, cell-based, and animal models. Analytical workflows involving chromatographic separation, mass spectrometry, and bioinformatic prediction have improved peptide discovery, but results remain difficult to compare because processing conditions and activity assays are not standardized. Available evidence suggests that amaranth proteins are promising sources of multifunctional peptides; nevertheless, these findings do not yet establish clinical efficacy. Future work should optimize extraction and identification methods, clarify sequence-structure-activity relationships, evaluate stability and intestinal absorption, compare genotypes and non-seed tissues, and conduct well-designed in vivo studies, safety assessments, and clinical trials. Scalable processing and formulation strategies will also be required before amaranth-derived peptides can be developed as reliable functional food, nutraceutical, or pharmaceutical ingredients.

Hepatic sinusoidal obstruction syndrome (HSOS) is a life-threatening liver vascular disorder with limited treatment options. HSOS results from the activation and injury of liver sinusoidal endothelial cells (LSECs). Berberine (BBR) has been shown to protect endothelial cells in various diseases. However, whether BBR can alleviate liver injury and LSEC disruption in HSOS remains unclear. In this study, we aimed to evaluate the effect of BBR on HSOS.

Two mouse models of HSOS were established using monocrotaline or oxaliplatin. Mice in the treatment groups received a low dose (100 mg/kg) or a high dose (200 mg/kg) of BBR daily. Histology, scanning electron microscopy, immunofluorescence, and flow cytometry were used to evaluate the therapeutic effects of BBR. Cell co-culture, Transwell assays, qRT-PCR, and Western blotting were performed to investigate the molecular pathways involved.

BBR treatment dose-dependently reduced liver injury and disruption of LSECs in murine HSOS models. Moreover, BBR significantly reduced hepatic neutrophil infiltration, thereby attenuating neutrophil-mediated injury to LSECs. Additionally, BBR inhibited the effect of injured LSECs on neutrophil activation. Mechanistically, injured LSECs were identified as one of the major sources of CXCL1 in HSOS, and BBR downregulated CXCL1 expression in injured LSECs by inhibiting MAPK signaling.

In this study, we demonstrate that BBR ameliorates HSOS by inhibiting endothelial-mediated neutrophil recruitment and activation. BBR may be a promising therapeutic option for HSOS treatment.