Intraoperative hypothermia is common during major surgery, but its economic implications in liver transplantation remain unclear. This study evaluated the association between intraoperative hypothermia and total hospitalization cost in adult liver transplant recipients. This single-center retrospective cohort study included adult liver transplant recipients who underwent transplantation between January 2020 and December 2025. Intraoperative hypothermia was defined as any recorded intraoperative core temperature < 36.0 °C. Multivariable linear regression with log-transformed total hospitalization cost was used to evaluate the association after adjustment for prespecified covariates. Sensitivity analyses used additional adjustment models and alternative temperature exposure metrics. Cost components were analyzed descriptively. Among 343 recipients, 239 (69.68

In this study, we evaluated the prognostic capacity of the lymphocyte-to-C-reactive protein ratio (LCR) in predicting one-year recurrence among patients with microvascular invasion (MVI)-positive hepatocellular carcinoma (HCC) who underwent postoperative adjuvant transarterial chemoembolization (PA-TACE). A total of 480 HCC patients were retrospectively enrolled in this single-center study. Among them, 146 patients with MVI-positive HCC underwent PA-TACE. The LCR was calculated prior to surgery using the formula: LCR = 104 × lymphocyte count (109/L) / C‑reactive protein (mg/L). The predictive value of LCR for early recurrence was assessed using LASSO regression, along with univariate and multivariate Cox regression analyses. A prognostic model was subsequently developed and validated through decision curve analysis (DCA) and receiver operating characteristic (ROC) curve analysis. In the nomogram model, an LCR value below 11,000 (≤ 11,000 vs. > 11,000; HR = 3.268, 95

In this study, the characteristics of the macrotrabecular-massive (MTM) hepatocellular carcinoma (HCC) subtype were analysed and summarized, and the prognostic value of postoperative adjuvant TACE for MTM-HCC was evaluated. This study enrolled 70 patients with the MTM subtype. In the study population, 44 patients underwent postoperative adjuvant TACE therapy, and 26 patients were included in the control group. Subsequently, 14 paired patients were analysed using propensity score matching (PSM). This study revealed that MTM-HCC exhibited higher AFP levels, poorer tumour differentiation, higher portal vein and MVI invasion rates, and larger tumours. In patients with MTM-HCC, univariate analysis revealed significant differences in the tumour diameter (t = 2.283; P = 0.026), microvascular invasion (MVI) (χ2 = 7.306; P = 0.007), and portal vein tumour thrombus (PVTT) (χ2 = 6.894; P = 0.009) between the TACE and control groups before matching. Survival analysis indicated that the 1-, 3-, and 5-year probabilities of OS and RFS in patients with MTM-HCC who received TACE were worse relative to patients who did not receive TACE before matching (P < 0.05). Consequently, a PSM analysis with 1:1 matching was performed for MVI, PVTT, and tumour diameter. After matching, no significant difference was noted between the two groups (P > 0.05). In addition, multivariate Cox regression analysis indicated that PVTT, TACE therapy, and multiple tumours were independent risk factors for OS, whereas the ALBI grade was an independent risk factor for RFS in patients with MTM-HCC. The efficacy of postoperative adjuvant TACE for MTM-HCC may fail because of the higher MVI and PVTT incidence and the larger tumour diameter associated with this histopathological subtype.

Background:Cirrhosis, particularly HBV-induced, poses a significant global health burden. This study compares immune cell landscapes in HBV and non-viral cirrhosis using single-cell RNA sequencing (scRNA-seq) to elucidate distinct immune mechanisms driving disease progression. Methods:Liver tissues from HBV cirrhosis patients and healthy controls were analyzed via scRNA-seq. Public single-cell and spatial transcriptomics data were integrated to map immune cell populations. Computational analyses included differential expression, pathway enrichment (KEGG/GO), and cell-cell communication (CellChat). Results:HBV cirrhosis exhibited expanded Macrophage-PLCG2 (anti-inflammatory) and CD8 + T-FABP5 subsets, while Macrophage-CD5L, CD4 + T-ANXA1, CD4 + T-CCR6, and NK-FCER1G were reduced. Pathway analysis linked Macrophage-PLCG2 to Rap1 signaling, whereas Macrophage-CD5L associated with lysosomal pathways. Spatial analysis revealed myeloid-T cell colocalization in HBV cirrhosis. Enhanced HLA-E/KLRK1 signaling between myeloid and NK cells was identified in HBV cases (p < 0.05). Conclusion:This study delineates immune cell heterogeneity between HBV and non-viral cirrhosis, highlighting potential therapeutic targets like Macrophage-PLCG2 and CD8 + T-FABP5. Findings underscore the role of immune dysregulation in HBV cirrhosis progression.

Liver regeneration after hepatectomy is a challenge in patients with metabolic dysfunction-associated steatohepatitis (MASH), as well as small-for-size syndrome and ex vivo organogenesis. Endogenous lipid metabolites promoting liver regeneration are poorly understood. A 70% partial hepatectomy (PHx) was performed in mice with healthy and MASH liver. Biomarkers promoting liver regeneration were explored using hepatic lipidomics followed by structural identification. The functional validation was performed in in vivo and in vitro models. Liver regeneration post-PHx peaked earlier in the MASH liver than that in the healthy liver. Phosphatidylcholine (PC) (16:0/20:4) increased in both MASH liver and non-MASH liver, and it promoted the proliferation of Hepa 1-6, Huh-7, human liver organoids, and mouse PHx models. In patients with metabolic dysfunction-associated steatotic liver disease (MASLD) and those undergoing hepatectomy, the serum PC (16:0/20:4) also increased, supporting the findings in this work. PC (16:0/20:4) is an endogenous lipid biomarker promoting liver regeneration which increased during hepatectomy in healthy and MASH liver.

Transcriptomic studies of liver preservation and ischemia-reperfusion injury (IRI) often report large gene lists that are difficult to translate into deployable diagnostic tools. Genome-wide profiling remains impractical within organ procurement timelines, where decisions must be made rapidly and assay infrastructure is limited. A compact, interpretable gene panel deployable via targeted platforms such as NanoString or RT-qPCR could bridge this gap between transcriptomic discovery and clinical utility. We asked whether full transcriptomes from human liver cohorts can be compressed into such panels without loss of classification performance. Seven GEO datasets covering static cold storage, hypothermic/normothermic machine perfusion, ischemic preconditioning, and peri-transplant biopsies (GSE112713, GSE276531, GSE12720, GSE14951, GSE15480, GSE151648_TIME, GSE151648_IRI) were re-processed into ML-ready expression and phenotype matrices. All gene identifiers were harmonized to HGNC symbols before any modelling step. For each dataset, elastic net (EN) logistic regression and XGBoost were trained and evaluated within a repeated nested cross-validation framework (fivefold × 3-repeat; 15 outer folds), with feature selection performed exclusively on the outer training partition. The union of the top-30 EN coefficient and top-30 XGBoost gain importance genes (EN ∪ XGB) was evaluated on the held-out outer test fold. Nested CV yielded AUCs of 0.842-0.965 across four datasets with reliable sample sizes (n ≥ 30). The two largest cohorts, GSE151648_TIME (n = 80) and GSE12720 (n = 42) achieved AUC = 0.959 ± 0.052 and 0.965 ± 0.059 respectively, with specificity and PPV > 0.90. GSE276531 (n = 32) did not yield reliable transcriptomic signal in either label orientation and is reported as a negative result. Cross-dataset transferability assessed by Leave-One-Dataset-Out validation was consistently poor, with balanced accuracy of 0.500 and macro F1 ≤ 0.333 in five of seven test sets, indicating majority-class collapse rather than genuine cross-dataset signal, suggesting that panels are largely context-specific. An exception was observed among the three reperfusion-focused cohorts (GSE12720, GSE15480, GSE151648_TIME), where high bidirectional panel transfer within this subset (AUC = 0.99-1.00) coincided with convergent selection of inflammatory, proteotoxic stress, and AP-1 axis genes across independently derived panels. Explainable ML models can compress liver transplant transcriptomes into compact, context-specific gene panels with strong within-cohort diagnostic accuracy. The convergence of biologically coherent gene signatures across reperfusion-focused cohorts lends biological support to these panels, while consistently poor LODO transfer underscores the need for cohort-tailored assay development and prospective validation.

BACKGROUND:Cholestatic liver injury involves impaired bile acid (BA) formation or flow, leading to toxic hepatic BA accumulation, yet the underlying mechanisms remain poorly understood. Leukocyte cell-derived chemotaxin 2 (LECT2) has been implicated in liver metabolic disorders; however, its specific role in cholestasis remains incompletely understood. METHODS:ANIT was administered to wild-type (WT) and LECT2 knockout (KO) mice to establish an intrahepatic cholestasis model. Metabolomics and metagenomics were performed to discover the role of BA metabolism and the gut-liver axis in cholestatic liver injury. Clinical samples were analyzed to assess the relationship between LECT2 and cholestatic liver injury. RESULTS:LECT2 deletion was associated with altered BA synthesis, characterized by a shift toward the classical pathway with upregulation of CYP7A1 and CYP8B1. Under cholestatic conditions, LECT2 deficiency was associated with aggravated liver injury, accompanied by alterations in gut microbiota composition, changes in intestinal FXR-FGF15 signaling, and increased hepatic JNK activation. In KO mice, HDCA supplementation restored the alternative synthesis pathway, FMT reshaped gut microbiota, and antibiotic cocktail treatment suppressed intestinal FXR signaling, each of which was associated with improved cholestatic liver injury. In clinical samples, LECT2 levels were negatively correlated with markers of cholestasis, supporting its potential relevance to disease severity. CONCLUSION:LECT2 deficiency is associated with aggravated cholestatic liver injury, which may involve altered BA synthesis, gut microbiota dysbiosis, and modulation of intestinal FXR-hepatic JNK signaling. These findings offer new insights into the role of LECT2 in regulating metabolism and identify potential therapeutic targets for managing cholestatic liver injury.

Liver transplantation (LT) is a complex procedure that results in multiple postoperative complications. Surgeons use the Clavien-Dindo classification (CDC) to evaluate the severity of complications; however, only a few studies have reported the use of the Comprehensive Complication Index® (CCI®) to evaluate complications associated with LT and split liver transplantation (SLT). This study explored the application of the CCI® to evaluate complications after whole liver transplantation (WLT) and SLT. During this retrospective study, 244 WLT and 104 SLT recipients were enrolled between January 2016 and June 2023. The clinical characteristics and postoperative complications (at hospital discharge) of the WLT and SLT groups were evaluated and compared. The median in-hospital CCI® score was 43.9. A comparison of the WLT and SLT groups indicated no significant differences in CCI® scores (WLT, 44.2; SLT, 43.3; p = 0.716). The postoperative intensive care unit stay and length of the postoperative stay were strongly correlated with the CCI® score of the entire cohort and those of the SLT and WLT groups (all p < 0.001). The CDC and CCI® demonstrated a Spearman’s rank-order correlation of 0.838 (p < 0.001). Additionally, the proportion of female recipients was significantly higher in the SLT group (25.0

The prognosis for patients diagnosed with hepatocellular carcinoma with bile duct tumor thrombus (HCC-BDTT) remains dismal, and there are presently no universally accepted treatment guidelines to address this complex condition. Long-term outcomes of liver transplantation (LT) for HCC-BDTT patients are unclear, and whether LT is a proper therapeutic option for HCC-BDTT patients remains to be determined. Therefore, we design a clinical trial to evaluate whether LT can improve recurrence-free survival (RFS) and overall survival (OS) in HCC-BDTT patients. This is an open-labeled, single-arm, prospective, multicenter and real-world study aiming to assess the survival outcomes of HCC-BDTT patients in LT. Patients will be enrolled based on histological confirmation of HCC with BDTT. The study is planned to take 4 years, 2 years for enrollment and 2 years for follow-up. We anticipate that LT confers beneficial survival outcomes for HCC-BDTT patients, specifically in terms of the pivotal parameters, such as RFS and quality of life. Upon successful completion of the trial, we will extend our monitoring over a longer follow-up time to accurately estimate important indicators such as OS. We expect that this study provides substantial evidence to refine treatment guidelines through thorough data analysis, ultimately contributing to better patient outcomes and advancing our understanding of the disease.Trial Register: Trial registered at www.clinicaltrials.gov (NCT06928415)

Background: Up to 30–50% of patients with ulcerative colitis (UC) fail biologic therapy, yet reliable tissue-level predictors of response are lacking and the full-thickness pathology of medically refractory UC remains poorly defined. We aimed to map the spatial microenvironment of refractory UC across the entire colonic wall and to derive niche-specific signatures that predict biologic treatment outcome. Methods: We performed 10x Visium HD spatial transcriptomics (16-µm bins; 615,274 bins) on full-thickness colonic resections from three medically refractory UC patients and three controls. Niche-stratified differential expression, spatial cell–cell communication, SCENIC regulon inference and single-sample GSEA were combined with immunofluorescence and DSS-colitis flow cytometry. Niche signatures were tested as predictors of biologic non-response or non-remission across seven independent cohorts by ROC analysis, leave-one-out cross-validation and cross-cohort external validation. Findings: We resolved 18 spatial niches across five tissue modules, revealing mucosal barrier collapse with a 20-fold expansion of ulcer-bed stroma (p=0.030) and a submucosal humoral programme with tertiary lymphoid structures (TLS). An Acute Neutrophil Niche signature predicted biologic non-response with areas under the curve of 0.67–0.99 across six adult cohorts and non-remission in the paediatric PROTECT cohort; a five-niche model generalised across datasets and drug classes (external-validation AUC 0.68–0.97). TNFAIP2⁺ TLS B-cell expansion was confirmed by immunofluorescence and cross-species flow cytometry (p=0.0079). Interpretation: This full-thickness spatial atlas of refractory UC yields externally validated, drug-class-agnostic cellular-niche biomarkers, providing a spatially grounded framework to support personalised biologic therapy selection in UC, pending prospective validation.

Purpose:Circular RNAs (circRNAs) have been shown to have critical regulatory roles in hepatocellular carcinoma (HCC). This study aims to investigate the predictive value of circLZTR1 for early recurrence of HCC. Patients and Methods:In this study, circLZTR1 (a circRNA derived from the LZTR1, hsa_circ_0062403) was identified and validated in the HCC cohort. Univariate analyses and multivariate Cox regression were conducted to analyze the functional role of hsa_circ_0062403 in the postoperative early recurrence of HCC patients. Receiver operating characteristic curve (ROC) analysis was performed to assess the predictive performance of hsa_circ_0062403 for early recurrence. Results:91 patients with HCC after surgery were included. circLZTR1 was downregulated in early recurrence HCC patients and predicted poor recurrence-free survival (P=0.029). In addition, a significant downregulation of circLZTR1 was observed in HCC from patients with MVI or PVTT. Multivariate Cox regression analysis indicated that lower circLZTR1 (>0.25 vs <0.1; HR = 0.142, 95% CI: 0.042-0.482, P = 0.002), higher AFP (>400 vs <20; HR = 7.880, 95% CI: 2.499-24.844, P < 0.001), higher INR (HR = 4.203, 95% CI: 1.133-15.588, P = 0.032), multiple tumors (HR = 3.795, 95% CI: 1.541-9.346, P = 0.004), PVTT positive (HR = 3.438, 95% CI: 1.050-11.258, P = 0.041), and larger tumor diameter (HR = 1.306, 95% CI: 1.101-1.550, P = 0.002) served as independent risk factor for early recurrence of HCC. ROC analysis indicated that the Cox model demonstrated higher sensitivity and specificity than the clinical model and single circLZTR1 in prediction for early recurrence of HCC patients (AUC = 0.767, 95% CI: 0.666-0.868, P < 0.001). Conclusion:The downregulation of circLZTR1 is closely associated with the acquisition of invasive phenotypes, vascular invasion, and subsequent early recurrence of HCC patients, suggesting that circLZTR1 may serve as a novel prognostic biomarker for predicting early recurrence in patients with HCC.

Cold preservation is a critical logistical step in liver transplantation but induces ischemia-reperfusion injury (IRI), a key driver of early graft dysfunction. While bulk tissue assays capture global damage, they obscure the cell-type-specific transcriptional programs engaged during hypothermic storage. We utilized a multicellular human liver-on-chip model comprising Patient-Derived Organoids (PDOs), hepatic stellate cells (HSCs), liver sinusoidal endothelial cells (LSECs), and macrophages. Chips were exposed to 24-h static cold storage using either the clinical standard University of Wisconsin (UW) solution or a hyperbranched polyglycerol (HPG)-based formulation, followed by normothermic reperfusion. Single-cell RNA sequencing (scRNA-seq) was performed to map transcriptional trajectories across the preservation-reperfusion axis. We identified candidate solution-dependent transcriptional differences across cell types. PDOs from UW-preserved chips showed comparatively higher mean expression of inflammatory and oxidative stress-associated transcripts (IFI27, SAA1, HMOX1) and mitochondrially-encoded genes (MT-ND5) relative to HPG-preserved samples, which retained comparatively higher expression of homeostatic epithelial markers (EPCAM, KRT18). HSCs and LSECs in the UW group showed comparatively elevated expression of fibrosis-associated (COL1A1, TAGLN) and endothelial adhesion (ICAM1) transcripts. Ligand-receptor interaction modelling identified candidate inflammatory communication axes, including chemokine signaling interactions (CXCL1, CCL20) between macrophages and epithelial compartments, with higher predicted activity under UW preservation. This study provides an exploratory, high-resolution map of cell-type-specific transcriptional patterns associated with hypothermic preservation in a liver-on-chip model. Our findings suggest that preservation solution chemistry is associated with distinct transcriptional signatures spanning stress response, mitochondrial, and intercellular signaling pathways. Transcriptional patterns in HPG-preserved cells were consistent with comparatively attenuated injury responses; however, these observations are hypothesis-generating and require independent biological replication and functional validation, including metabolic flux assays and ROS production measurements before conclusions regarding mitochondrial protection or clinical preservation efficacy can be drawn.

Background: Static measures of intraoperative hypothermia may not capture the timing and evolution of temperature changes during liver transplantation. This study aimed to identify intraoperative core temperature trajectory phenotypes and examine their association with early allograft dysfunction (EAD). Methods: This single-center retrospective cohort study included adult liver transplant recipients treated between January 2016 and December 2025. Core temperature was recorded at 5-min intervals. An 18-point hybrid landmark sequence was constructed to align temperature measurements with operative phases, and latent growth mixture modeling was used to identify trajectory classes. The primary outcome was EAD. Associations between trajectory class and EAD were assessed using hierarchical logistic regression models adjusted for recipient, donor–graft, and intraoperative stress factors. Peri-reperfusion AUC below 36°C was evaluated as a complementary measure of hypothermic burden. Results: Among 519 eligible patients, 518 had valid temperature trajectory classification. Four trajectory phenotypes were identified. Classes 1 and 2 showed lower temperatures around reperfusion and were associated with higher odds of EAD before adjustment for intraoperative stress variables. After further adjustment for intraoperative stress factors, these associations were attenuated and were no longer statistically significant. Class 1 had higher intraoperative stress across hemodynamic, transfusion-related, metabolic, and perfusion-related domains. Peri-reperfusion AUC below 36°C showed a similar attenuation pattern. Conclusions: Intraoperative temperature trajectory phenotypes were associated with EAD before adjustment for intraoperative stress variables, but this association was attenuated after accounting for intraoperative stress. Lower-temperature peri-reperfusion trajectories may reflect concomitant physiological stress rather than isolated thermal exposure. External validation is required to determine their value for peri-reperfusion risk recognition.

The restoration of liver mass after partial hepatectomy (PH) and split liver transplantation (SLT) relies on efficient liver regeneration, a process highly susceptible to metabolic dysregulation. Although remodeling of the tricarboxylic acid (TCA) cycle is commonly observed during liver injury and regeneration, the specific role of succinic acid remains unclear. Here, we integrated radiomics, transcriptomics, metabolomics, and functional assays to systematically evaluate the association between succinic acid and liver regeneration. Multi-omics analysis of 20 SLT patients demonstrated that elevated succinic acid levels were strongly associated with impaired regenerative outcomes, and weighted gene co-expression network analysis identified the TCA cycle as a key regeneration-associated metabolic module. In a 70

Background: Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with poor prognosis and limited therapeutic options. A disintegrin and metalloproteinase 12 (ADAM12) is aberrantly expressed in multiple cancers and has been implicated in tumor progression. However, its biological role and underlying mechanism in HCC remain unclear. Methods: Public HCC datasets and bioinformatics analyses were used to evaluate ADAM12 expression and its clinical significance. The effects of ADAM12 on HCC cell viability, colony formation, migration, invasion, and apoptosis were assessed in vitro, and its role in tumor growth was examined in a xenograft model. The underlying mechanism was investigated by immunoprecipitation-mass spectrometry, co-immunoprecipitation, cycloheximide chase, ubiquitination, and metabolic assays. Results: ADAM12 was significantly upregulated in HCC tissues and was associated with unfavorable overall survival. ADAM12 knockdown inhibited cell viability, colony formation, migration, and invasion, promoted apoptosis in vitro, and suppressed xenograft tumor growth in vivo without obvious body weight loss. Mechanistically, EIF3B was identified as an ADAM12-interacting protein. ADAM12 knockdown decreased EIF3B protein abundance without affecting its mRNA level, accelerated EIF3B degradation, and increased its ubiquitination, indicating that ADAM12 stabilizes EIF3B by limiting ubiquitin-proteasome-mediated degradation. Moreover, ADAM12 depletion reduced PKM2 and LDHA expression, decreased extracellular acidification rate, lactate production, and glucose uptake, and increased oxygen consumption rate, indicating a shift from glycolysis toward oxidative phosphorylation. These effects were largely rescued by EIF3B overexpression or PKM2 restoration. Conclusion: ADAM12 promotes glycolytic reprogramming and tumor progression in HCC by stabilizing EIF3B and regulating the EIF3B/PKM2 axis. The ADAM12-EIF3B pathway may therefore represent a potential therapeutic target in HCC.

Background:Full-size split liver transplantation (FSLT) offers an attractive way to expand the donor pool for adult patients. However, the efficacy and safety of FSLT remain under debate. Materials and Methods:One hundred and three recipients who underwent FSLT were enrolled, and 124 recipients who received whole-liver transplantation (WLT) were taken as a control group. Clinical data and short-term outcomes within 1 year posttransplantation from 2019 to 2023 were compared between the two groups. Survival rates were calculated using the Kaplan-Meier method and compared by the log-rank test. Meanwhile, propensity-score matching (PSM) using key prognostic factors was conducted and the results were compared. Univariate and multivariate logistic regression analyses were performed to identify risk factors for serious complications in FSLT. Results:Thirty-three (29.2%) and 25 (20.2%) recipients in FSLT and WLT experienced postoperative complications graded ≥ III, with no significant differences (P = 0.106). However, biliary and vascular complications were more frequent in FSLT than in WLT (11.5% vs. 4.0% and 12.4% vs. 1.6%). The 3- and 6-month mortality rates in FSLT did not differ significantly from those in WLT (6.2% and 8.8% vs. 3.2% and 4.8%). The 1-year recipient (OS) and graft survival (GS) rates were 87.6% and 85.8% for FSLT, and 92.7% and 91.9% for WLT, with no significant differences. After PSM, the 1-year OS and GS were 81.3% and 81.3% for FSLT, and 90.6% and 90.6% for WLT (P = 0.081). Multivariate analysis revealed that a graft with steatosis of 5%-10%, a MELD score ≥ 20, sarcopenia, a history of hepatectomy, and an operation time > 420 min were independent risk factors for the incidence of postoperative complications graded ≥ III in FSLT. Conclusions:FSLT remains a challenging procedure. However, the short-term outcomes of FSLT were acceptable compared with those of WLT, encouraging the use of this procedure to increase the donor pool whenever possible.

BACKGROUND:Sarcopenia is associated with poor prognosis in liver transplantation, but the prognostic value of broader body composition indicators in patients undergoing liver transplantation for hepatocellular carcinoma requires further investigation. This study aimed to explore their critical role in the precision evaluation system. METHODS:Consecutive cases from four centers between January 2015 and January 2022 were included. Pre-transplant abdominal computed tomography images were analyzed to assess body composition indicators, including skeletal muscle index (SMI), skeletal muscle radiation attenuation (SMRA), visceral adipose tissue index (VATI), and subcutaneous adipose tissue index (SATI). Survival analysis and Cox regression were performed to investigate the predictive efficacy of body compositions in recurrence-free survival (RFS), with interaction terms for Milan criteria status. A scoring model was developed using Framingham Heart Study methodology. RESULTS:A total of 700 male recipients were enrolled. Among all body composition indicators, low SMI (called sarcopenia) and low SMRA (called myosteatosis) were associated with worse 2-year RFS regardless of Milan criteria status, whereas low VATI (P = 0.002) and low SATI (P = 0.001) were associated with worse RFS only in recipients exceeding the Milan criteria. These body composition indicators exhibited cumulative adverse effects on outcomes. Further analysis revealed significant interactions between Milan criteria status and sarcopenia, as well as low SATI. A body composition-based scoring model was developed, defining three risk classes with a C-index of 0.70 [95 % confidence interval (CI): 0.67-0.72], which significantly improved the predictive efficacy for recurrence compared to conventional criteria. Notably, using marginal liver was a risk factor for RFS in moderate risk patients (62.8 % vs. 48.8 %, P = 0.024). CONCLUSIONS:This model highlights the prognostic value of body composition in liver transplantation for hepatocellular carcinoma and provides a refined predictive model to enhance recurrence risk assessment. The findings offer valuable insights for defining marginal liver utilization and developing effective treatment strategies.

Effective biomarkers for predicting early recurrence (ER) (within one-year post-surgery) of hepatocellular carcinoma (HCC) are lacking. LZTR1, a known tumor suppressor, plays a role in HCC development. This study investigated the correlation between LZTR1 expression and ER of HCC and its effects on HCC cells. Clinical data of 101 HCC patients were collected to evaluate tumor prognostic factors. ROC curve analysis was used to evaluate the predictive ability of LZTR1 in HCC. Huh7 cells and SK-Hep-1 cells were used for cell experiments to observe the effects of knocking out LZTR1 on tumor cell proliferation and metastasis. Cox analysis showed that alpha-fetoprotein (P = 0.010), LZTR1 (P = 0.014), tumor number (P = 0.032), and portal vein tumor thrombus (P = 0.001) as independent factors associated with ER of HCC. The one-year recurrence-free rate of HCC patients with high LZTR1 expression (≥ 1.7) was 73.2

Background/Objectives: Liver-on-a-chip (LiOC) technology is increasingly recognized as a transformative platform for modeling liver biology, disease mechanisms, drug metabolism, and toxicity screening. Traditional two-dimensional (2D) in vitro models lack the complexity needed to replicate the liver’s unique microenvironment. This review aims to summarize recent advancements in LiOC systems, emphasizing their potential in biomedical research and translational applications. Methods: This narrative review synthesizes findings from key studies on the development and application of LiOC platforms. We explored innovations in material science and bioengineering, including microfluidic design, 3D printing, stem cell– and tissue-derived liver organoid integration, and co-culture strategies. Commercially available LiOC systems and their regulatory relevance were also evaluated. Results: LiOC systems have evolved from simple PDMS-based chips to complex, multicellular constructs incorporating hepatocytes, endothelial cells, Kupffer cells, and hepatic stellate cells. Recent studies demonstrate their superior ability to replicate liver-specific architecture and functions. Applications span cancer research, drug toxicity assessment (e.g., drug-induced liver injury prediction with >85% sensitivity), disease modeling, and regenerative medicine. Several platforms have gained FDA recognition and are in active use for preclinical drug testing. Conclusions: LiOC technology offers a more physiologically relevant alternative to traditional models and holds promise for reducing reliance on animal studies. While challenges remain, such as vascularization and long-term function, ongoing advancements are paving the way toward clinical and pharmaceutical integration. The technology is poised to play a key role in personalized medicine and next-generation therapeutic development.

OBJECTIVE:Hepatitis B virus (HBV) remains an important risk factor for hepatocellular carcinoma (HCC), and inflammation plays an essential role in tumor development. This study aimed to investigate the impact of inflammatory markers in the postoperative outcomes of patients with HBV-related HCC, providing valuable prognostic indicators after hepatectomy. METHODS:We retrospectively analyzed 222 patients with HBV-related HCC after surgical resection. The ROC curve was used to calculate biomarker cutoff values. The Kaplan-Meier method was used to estimate overall survival (OS) and recurrence-free survival (RFS), and univariate and multivariate analyses were used to identify the prognostic factors. RESULTS:The Kaplan-Meier analysis revealed that patients with high albumin-bilirubin (ALBI) score, aspartate aminotransferase to platelet ratio index (APRI), and monocyte to lymphocyte ratio (MLR) had worse OS, while those with high ALBI score and MLR had shorter RFS. Multivariate Cox regression analysis identified alpha-fetoprotein >400 ng/mL (hazard ratio [HR]: 2.447, 95% confidence interval [CI]: 1.273-4.706, p = 0.007), alanine aminotransferase (HR: 0.377, 95% CI: 0.171-0.834, p = 0.016), platelet to lymphocyte ratio (HR: 0.385, 95% CI: 0.196-0.755, p = 0.006), systemic inflammatory response index (HR: 1.844, 95% CI: 1.049-3.239, p = 0.033), ALBI score (HR: 1.808, 95% CI: 1.020-3.203, p = 0.043), APRI score (HR: 3.193, 95% CI: 1.662-6.137, p < 0.001), tumor diameter (HR: 1.083, 95% CI: 1.012-1.160, p = 0.022), and portal vein tumor thrombosis (PVTT) (HR: 6.083, 95% CI: 2.774-13.338, p < 0.0001) as independent predictors for OS. MLR (HR: 2.285, 95% CI: 1.290-4.048, p = 0.005) and PVTT (HR: 2.672, 95% CI: 1.280-5.579, p = 0.009) were confirmed as significant prognostic markers of RFS in patients with HBV-related HCC. CONCLUSIONS:ALBI score, APRI, and MLR are effective prognostic predictors in patients with HBV-related HCC after curative resection. Close monitoring and adjuvant therapies should be considered for high-risk patients.