The clinical spectrum from cirrhosis to hepatocellular carcinoma (HCC) reflects interactions among hepatic dysfunction, systemic inflammation, and tumor burden. Whether circulating biomarkers add value beyond clinical parameters remains uncertain. This study aimed to evaluate an exploratory Model for End-Stage Liver Disease (MELD)–neutrophil-to-lymphocyte ratio (NLR)-based clinical–inflammatory phenotyping framework for discriminating advanced HCC features and to determine whether circulating hsa_circ_101555 provides incremental discriminatory value beyond this framework.

This single-center cross-sectional study included 92 consecutive patients (30 with cirrhosis without HCC and 62 with HCC). Patients were classified into three exploratory clinical–inflammatory phenotypes using a hierarchical MELD–NLR algorithm (Phenotype I, n = 25; II, n = 33; III, n = 34). Circulating hsa_circ_101555 was quantified by reverse transcription quantitative polymerase chain reaction. Receiver operating characteristic analysis evaluated Barcelona Clinic Liver Cancer stage C among patients with HCC (n = 62; events = 28). Internal validation used bootstrap resampling.

Higher-risk phenotypes included progressively larger proportions of patients with HCC and greater frequencies of advanced tumor characteristics. The combined MELD–NLR model showed the highest discrimination (the area under the receiver operating characteristic curve (AUC) 0.90; 95% confidence interval 0.82–0.97), with 85.7% sensitivity, 82.4% specificity, and 83.9% accuracy. This performance exceeded that of NLR alone (AUC, 0.80) and MELD alone (AUC, 0.77). Circulating hsa_circ_101555 was associated with smaller tumors and an earlier Barcelona Clinic Liver Cancer stage but showed modest discrimination (AUC, 0.69) and did not improve the MELD–NLR model (ΔAUC = 0.002; DeLong P = 0.79).

The exploratory MELD–NLR-based clinical–inflammatory framework identifies patient groups with differing frequencies of advanced HCC features. Circulating hsa_circ_101555 provides no incremental discriminatory value beyond routinely available clinical–inflammatory parameters and requires external validation before clinical use.

Although hepatitis B surface antigen (HBsAg)-specific B cells have been partially characterized in chronic hepatitis B (CHB), the role of Naïve B cells and their potential relevance to functional cure remain insufficiently explored. Here, we aimed to characterize the naïve B-cell subsets between cured and uncured patients with CHB.

In this retrospective study, we applied single-cell RNA sequencing to compare peripheral B-cell profiles between cured and uncured CHB patients. Key findings were validated by flow cytometry in an independent cohort and further supported in a nucleos(t)ide analog monotherapy cohort stratified by HBsAg levels.

Single-cell RNA sequencing characterized two Naïve B-cell subsets, designated IL-4R+SELL+ and IL-4R−SELL− Naïve B cells, which were differentially distributed between functionally cured and uncured patients. Cured patients showed higher frequencies of total B cells and IL-4R+SELL+ Naïve B cells than uncured patients. In contrast, uncured patients exhibited persistent hyperactivation of type I interferon signaling in both Naïve and memory B cells. The IL-4R+SELL+ subset showed a transcriptional signature associated with germinal center biology and exhibited stronger ligand–receptor interactions with CD40LG+CD4+ T cells. Notably, the frequency of the IL-4R+SELL+ subset was inversely correlated with HBsAg levels. Consistently, patients with lower HBsAg levels also exhibited significantly higher frequencies of IL-4R+SELL+ Naïve B cells compared with those with high HBsAg levels.

Collectively, these findings indicate that the IL-4R+SELL+ Naïve B-cell subset is characterized by germinal center-related responses and enhanced T-cell-mediated help and may serve as an immunological component associated with functional cure in CHB.

Biliary atresia (BA) is the leading cause of pediatric obstructive cholestasis and a major indication for liver transplantation in infants. Organoid models are increasingly used to investigate BA pathogenesis and therapeutic responses, but incomplete methodological and clinical reporting may limit cross-study comparison and translational interpretation. This study aimed to map the landscape of BA-related organoid research, identify major reporting gaps, and propose Biliary Atresia Minimum Reporting Standard (BA-MRS) as a preliminary framework for improving reporting completeness.

PubMed, Scopus, and Web of Science Core Collection were searched on March 8, 2026, in accordance with the PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews) and the 2024 Joanna Briggs Institute (JBI) Manual for Evidence Synthesis. Reporting completeness was assessed using a 36-item BA-MRS across six domains, scored as fully reported, partially reported, not reported, or not applicable.

Twenty-six studies published between 2020 and 2026 were included. Fibrosis and epithelial–mesenchymal transition were the most frequently studied themes, whereas only one study linked organoid findings to post-Kasai outcomes. BA case/model definition, ethics approval, and differentiation protocols were fully reported in all applicable studies (100%). In contrast, contamination monitoring (3.8%), core biliary function assays (34.6%), and clinical outcome linkage (26.3%) were poorly reported. Culture System and Sample Acquisition showed the lowest domain-level fully reported rates (58.1% and 63.2%, respectively).

BA organoid research has progressed beyond early model development, but reporting remains insufficient for robust comparison, reproducibility, and clinically meaningful interpretation. BA-MRS may serve as a preliminary framework for improving standardized reporting in future studies.

Bilateral above-knee amputation stump ulcers with poor arterial inflow, multidrug-resistant infection, and bone involvement are rare and difficult to manage. We report a 52-year-old man who developed nonhealing bilateral stump ulcers more than one month after emergency bilateral amputation for extensive aortoiliac and lower-extremity arterial thrombosis. On admission on January 6, 2026, the right stump wound measured approximately 16.0 × 13.0 cm, with exposed femoral bone, purulent medullary drainage, and necrotic tissue; the left measured 18.0 × 12.0 cm, with slough and persistent exudation. Wound culture yielded carbapenem-resistant Klebsiella pneumoniae, and right femoral bone pathology supported chronic necrotizing osteomyelitis. Because immediate revascularization was not feasible, we used a staged debridement strategy—repeated selective debridement preserving viable tissue, with negative pressure wound therapy (NPWT) as a bridge between operations—combined with delayed stump repair, culture-guided antimicrobial therapy, anticoagulation, analgesia, vascular protection, and nutritional support. NPWT was applied in seven cycles over approximately 54 days. The wounds achieved complete closure by discharge on March 16, 2026. At follow-up on March 30, 2026, there was no exudation, sinus tract, recurrent dehiscence, exposed bone, recurrent infection, or significant stump pain, although prosthetic fitting was not yet possible. This case suggests that NPWT combined with serial staged debridement may offer short-term salvage for selected complex infected amputation stumps when arterial inflow is poor and one-stage closure is unsafe; however, durability and generalizability remain uncertain.

Hepatitis B virus (HBV) vertical transmission remains a major health challenge, and the characteristics of the placental immune microenvironment in chronic infection remain unclear. This study aimed to use mass cytometry to comprehensively analyze phenotypic changes in placental immune cell subsets.

We collected placental tissues from 20 pregnant women (6 healthy controls and 14 with chronic HBV infection). CD45+ leukocytes were detected using a 35-marker antibody panel. Unsupervised clustering identified 14 clusters, of which 13 immune clusters were analyzed.

HBV mainly caused functional remodeling of placental immune cells rather than changes in cell composition (P > 0.05 for all subsets). In natural killer (NK) cells, CD38 (P = 0.015) and CD16 (P = 0.0020) were notably upregulated and strongly correlated (ρ = 0.872, P < 0.001), suggesting potentially enhanced ADCC function. T cells showed upregulation of CD27, CD38, and CXCR5. Basophils exhibited the most pronounced changes: 9 differential markers (including chemokine receptors CCR4 and CCR7) were consistently downregulated. Classical monocytes showed an M1 polarization tendency (CD38↑, CD163↓). All P-values were raw; no markers remained significant after false discovery rate correction at an FDR threshold of < 0.1, indicating nominal significance. In addition, the coordinated expression patterns of markers within multiple cell subsets were weakened after infection.

These exploratory findings suggest that HBV may reshape placental immunity through enhanced NK cell activation, broad basophil suppression, and disrupted marker coordination. The sample size was limited (n = 20), so the results need to be validated in larger cohorts. These findings provide new perspectives for understanding the mechanisms of mother-to-child transmission.

Inter-individual variability in drug efficacy and toxicity remains a major obstacle to precision therapeutics. Candidate-gene pharmacogenomics and star-allele-based guidelines have established clinically useful examples, but they cannot capture the full spectrum of mechanisms that shape drug response. Pharmacogenomic genome-wide association studies (pharmacoGWAS) extend this framework by enabling discovery beyond known pharmacogenes and can identify human genetic variants associated with efficacy, adverse drug reactions, dose requirements, pharmacokinetics, and pharmacodynamics. This mini-review aims to summarize practical principles for human pharmacoGWAS, with emphasis on study design, phenotype and exposure definition, reproducible bioinformatics pipelines, gene-expression-based functional interpretation, and clinical translation. This review discusses randomized trials, prospective cohorts, biobanks, electronic health records, claims databases, and rare adverse-event designs, highlighting the specific biases that arise because drug response is defined among exposed individuals. It then outlines core analytical steps, including genotype quality control, imputation, ancestry-aware association testing, mixed models, survival and longitudinal analyses, rare-variant aggregation, replication, and meta-analysis. Particular attention is given to expression quantitative trait loci, splicing quantitative trait loci, and protein quantitative trait loci, tissue prioritization informed by the Genotype-Tissue Expression project, transcriptome-wide association studies, and colocalization as tools for prioritizing candidate genes and plausible mechanisms. Finally, we propose a translation framework connecting discovery to clinical validity, guideline development, electronic health record decision support, and equitable implementation across diverse populations. When combined with rigorous epidemiology and functional genomics, pharmacoGWAS may help translate genome-wide signals into safer and more effective prescribing.