iLIVER最新文献

{"title":"Salvage robotic associating liver partition and portal vein ligation for staged hepatectomy for advanced hepatocellular carcinoma with insufficient future liver remnant after conversion therapy","authors":"Wenliang Tan,&nbsp;Jinxing Wei,&nbsp;Xuan Luo,&nbsp;Yuxin Xiao,&nbsp;Yonglin Hua,&nbsp;Yajin Chen,&nbsp;Changzhen Shang","doi":"10.1016/j.iliver.2026.100256","DOIUrl":"10.1016/j.iliver.2026.100256","url":null,"abstract":"<div><div>Many cases of hepatocellular carcinoma (HCC) are initially considered unresectable. Advances in conversion therapy have enabled some of these patients to subsequently undergo curative resection. However, an insufficient future liver remnant (FLR) prevents patients with HCC undergoing conversion therapy from obtaining the opportunity for surgical resection. Associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) has been shown to be effective in promoting FLR hypertrophy in patients with HCC. Nevertheless, the safety and feasibility of ALPPS in patients with HCC who have an insufficient FLR after conversion therapy have rarely been reported. Here, we report the first case in which salvage robotic ALPPS enabled a patient with HCC and insufficient FLR after conversion therapy to undergo radical resection. This 56-year-old man was diagnosed with initially unresectable HCC and received five cycles of lenvatinib plus pembrolizumab. Although a partial response was achieved on oncological evaluation, the patient was not eligible for surgical resection because the FLR remained insufficient at 35.5% of the standard liver volume. To promote FLR hypertrophy and achieve radical resection, we performed a two-stage robotic ALPPS after the fifth cycle of systemic therapy. The FLR increased from 35.5% to 49.4% one month after the first stage of ALPPS (robotic cholecystectomy, right portal vein ligation, and liver partition), and subsequent robotic right hemihepatectomy was successfully performed. The patient recovered uneventfully after the two-stage procedure, and no recurrence was observed at the 3-month postoperative follow-up. This case demonstrates that total robotic ALPPS is a feasible bridge to curative resection for selected patients with insufficient FLR after successful conversion therapy. Building upon the concept of salvage ALPPS, this report further highlights the technical advantages of a total robotic platform in facilitating precise, minimally invasive staged hepatectomy.</div></div>","PeriodicalId":100657,"journal":{"name":"iLIVER","volume":"5 3","pages":"Article 100256"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148936402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the role of hypoxia inducible factors in liver fibrosis and future therapeutic applications","authors":"Yasha Taimuri,&nbsp;Riaz Ahmad","doi":"10.1016/j.iliver.2026.100260","DOIUrl":"10.1016/j.iliver.2026.100260","url":null,"abstract":"<div><div>Liver fibrosis is a chronic and progressive outcome of liver injury and continues to be a major contributor to liver morbidity and mortality. It is characterized by the excessive accumulation of extracellular matrix, resulting in the loss of normal liver architecture. Chronic liver injury also affects the availability of oxygen in the liver tissue, resulting in a hypoxic microenvironment. Among the major mediators of the hypoxic response, hypoxia-inducible factor-1α (HIF-1α) has been identified as a major regulator of fibrogenesis. The major experimental and clinical data have shown that the HIF pathway is closely linked to the activation of hepatic stellate cells, inflammation, pathological angiogenesis, and metabolic derangements in the fibrotic liver. These events are interlinked and result in the promotion of ongoing matrix accumulation and tissue remodeling. Recent studies have also indicated that the hypoxic pathways may cross-talk with ferroptosis and iron-mediated oxidative damage, providing new information on the mechanisms underlying the progression of fibrosis. This review aims to provide an overview of the current evidence on the role of HIF-1α in liver fibrosis and its connection between the major profibrotic pathways. We also provide information on the new therapeutic approaches targeting hypoxia signaling, including pharmacological inhibitors, von hippel-lindau (VHL) pathway modulation, and naturally derived compounds that have been reported to possess antifibrotic activity. A better understanding of the mechanisms driven by hypoxia may provide new information for the development of more accurate and stage-specific therapies for chronic liver diseases.</div></div>","PeriodicalId":100657,"journal":{"name":"iLIVER","volume":"5 3","pages":"Article 100260"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148936038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global trends, health inequalities, and long-term projections concerning liver cancer mortality attributable to nonalcoholic steatohepatitis between 1990 and 2050","authors":"Yujiao Deng,&nbsp;Zixuan Xing,&nbsp;Jingyue Tan,&nbsp;Jian Zu,&nbsp;Yue Zhang,&nbsp;Xiaomeng Cui,&nbsp;Chongyu Zhang,&nbsp;Qiaoman Fei,&nbsp;Dou Qu,&nbsp;Zhanpeng Yang,&nbsp;Yajing Bo,&nbsp;Enrui Xie,&nbsp;Yunyu Zhao,&nbsp;Xinyuan He,&nbsp;Xiao Yuan,&nbsp;Chenyang Qiao,&nbsp;Kairuo Wang,&nbsp;Xu Gao,&nbsp;Si Yang,&nbsp;Yuan Wang,&nbsp;Fanpu Ji","doi":"10.1016/j.iliver.2026.100258","DOIUrl":"10.1016/j.iliver.2026.100258","url":null,"abstract":"<div><h3>Background and aims</h3><div>Nonalcoholic steatohepatitis is an important and increasing contributor to liver cancer. This study investigated mortality trends in liver cancer attributable to nonalcoholic steatohepatitis (LCN) over recent decades and projected to 2050.</div></div><div><h3>Methods</h3><div>Spatiotemporal trends in age-standardized mortality rates (ASMRs) for LCN were evaluated using a Bayesian model. The Bayesian Age–Period–Cohort model was used to predict the ASMR and mortality in 2022–2050. Temporal trends were analyzed by calculating the average annual percent change (AAPC) in ASMRs. Health inequalities, frontier analysis, and decomposition analysis were applied.</div></div><div><h3>Results</h3><div>Between 1990 and 2021, the ASMR for LCN trended upwards worldwide (AAPC 0.82). The Americas had the most rapid growth in ASMR for LCN (AAPC 2.03), whereas the African region had the highest ASMR for LCN. By 2050, India (ASMR 0.76) and Indonesia (ASMR 0.50) are predicted to be among the most populous countries facing the highest ASMR burden. Health inequalities associated with a lower sociodemographic index value have worsened over time: the concentration index was −0.24 in 2021, and the slope index of inequality is projected to decline sharply from −0.33 in 2021 to −0.82 by 2050. Decomposition analysis showed that the increase in LCN mortality was mainly attributable to changes in epidemiology and age structure. The mortality burden of smoking and high fasting plasma glucose-related LCN has continued to rise over the last three decades.</div></div><div><h3>Conclusion</h3><div>Global LCN mortality is escalating, particularly in low-sociodemographic and low-income regions. The expanding mortality burden associated with smoking and high fasting plasma glucose underscores the importance of lifestyle and metabolic risk factors in shaping future trajectories and the need for targeted prevention strategies in high-burden regions.</div></div>","PeriodicalId":100657,"journal":{"name":"iLIVER","volume":"5 3","pages":"Article 100258"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148936039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional vulnerability and all-cause mortality among community-dwelling United States adults with a history of hepatitis or chronic liver disease","authors":"Chukwuemeka E. Ogbu,&nbsp;Ifeanyi Momodu,&nbsp;Philip N. Okafor","doi":"10.1016/j.iliver.2026.100259","DOIUrl":"10.1016/j.iliver.2026.100259","url":null,"abstract":"<div><h3>Background and aims</h3><div>Frailty predicts death in advanced cirrhosis and among transplant candidates, but whether a frailty-like functional index identifies mortality risk in the far larger population of community-dwelling adults with liver disease, who are rarely assessed for it, is unsettled. We examined whether a survey-based functional vulnerability index (FVI) was associated with all-cause mortality among US adults reporting a history of hepatitis or a chronic liver condition, independent of poverty and insurance status.</div></div><div><h3>Methods</h3><div>Retrospective cohort study using the National Health Interview Survey (2008–2018) linked to the National Death Index through December 31, 2019. Adults 18 years or older reporting a history of hepatitis or a chronic liver condition, eligible for mortality linkage, and without baseline liver cancer were included. The FVI was defined as the proportion of 9 self-reported deficits present (fair/poor self-rated health, ADL or IADL difficulty, work limitation; and difficulty walking, climbing, standing, carrying, or grasping), modeled per 0.10-unit higher score and by deficit count (0, 1, 2, or ≥ 3). Survey-weighted Cox models estimated hazard ratios (HRs) for all-cause mortality, and survey-weighted modified Poisson models estimated 5-year mortality risk ratios.</div></div><div><h3>Results</h3><div>Among 9291 adults (1151 deaths; 59,732 person-years; mean follow-up of 6.4 years), 64.6% had no functional deficit. In the fully adjusted model, each 0.10-unit higher FVI was associated with higher mortality (HR: 1.19, 95% confidence interval [CI]: 1.15–1.22), corresponding to an HR of 1.56 (95% CI: 1.44–1.68) per 1 − SD higher FVI. Versus no deficit, mortality increased with increasing burden: 1 deficit (HR: 1.37, 95% CI: 1.05–1.80); 2 deficits (HR: 2.49, 95% CI: 1.86–3.33); and ≥3 deficits (HR: 3.29, 95% CI: 2.65–4.08). Weighted 5-year mortality increased from 3.2% with no deficit to 23.0% with ≥3 deficits. The association was nonproportional and strongest during the first 2 years (HR: 1.28, 95% CI: 1.22–1.35), but persisted beyond 5 years (HR: 1.12, 95% CI: 1.07–1.18). Multiple imputation yielded similar results (HR: 1.20, 95% CI: 1.17–1.23). Poverty predicted mortality before but not after FVI adjustment; uninsurance did not.</div></div><div><h3>Conclusion</h3><div>Among community-dwelling US adults with hepatitis or chronic liver disease, a survey-based functional index was strongly and gradually associated with all-cause mortality, capturing risk not explained by poverty or insurance status. Brief functional assessment may identify high-risk patients well outside the transplant clinic.</div></div>","PeriodicalId":100657,"journal":{"name":"iLIVER","volume":"5 3","pages":"Article 100259"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148936401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone delactylation shapes epigenetic landscapes and therapeutic stratification in hepatocellular carcinoma","authors":"Zijie Wu ,&nbsp;Ximing Li ,&nbsp;Zhijun He ,&nbsp;Binghua Li ,&nbsp;Yanchao Xu ,&nbsp;Weiwei Hu ,&nbsp;Jintong Li ,&nbsp;Wenbing Yao ,&nbsp;Qiang Liu ,&nbsp;Xiangdong Gao ,&nbsp;Tao Jiang ,&nbsp;Hong Tian","doi":"10.1016/j.iliver.2026.100237","DOIUrl":"10.1016/j.iliver.2026.100237","url":null,"abstract":"<div><h3>Background and aims</h3><div>Histone lysine lactylation has emerged as a key epigenetic link between metabolism and gene regulation. Its homeostasis depends on both lactylation and delactylation. The biological and clinical relevance of histone lysine delactylation in hepatocellular carcinoma (HCC) remains unclear. This study aimed to investigate the clinical relevance of histone lysine delactylation (HLDL) in hepatocellular carcinoma and to establish an HLDL-based molecular classification for precision therapy.</div></div><div><h3>Methods</h3><div>We systematically profiled HLDL across multi-omics HCC cohorts (<em>n</em> &gt; 1700) to establish an HLDL-based molecular classification. Distinct subtypes were characterized by genomic, transcriptomic, and immune features. Therapeutic susceptibilities were predicted through pharmacogenomic modeling and validated by in vitro modulation of histone lysine lactylation.</div></div><div><h3>Results</h3><div>The HLDL classification delineated two major subtypes with distinct biological and therapeutic profiles. Low-HLDL tumors displayed higher genomic instability, activated oncogenic signaling, and an immune-infiltrated yet suppressive microenvironment, corresponding to poorer outcomes but higher sensitivity to immune checkpoint inhibitors, atezolizumab plus bevacizumab therapy, and sorafenib. In contrast, high-HLDL tumors exhibited a metabolically stable and delactylation-active phenotype, responding more favorably to lenvatinib and transarterial chemoembolization. Functional experiments confirmed that reduced HLDL activity led to elevated histone lysine lactylation, PD-L1 upregulation, and lenvatinib resistance, whereas restoring delactylation reversed these effects.</div></div><div><h3>Conclusions</h3><div>Histone lysine delactylation constitutes a critical epigenetic determinant of HCC heterogeneity and therapeutic response. The HLDL-based classification developed in this study integrates metabolic, immune, and pharmacologic features into a concise framework, offering new avenues for precision therapy and potential targets for modulating the lactylation-delactylation balance in HCC.</div></div>","PeriodicalId":100657,"journal":{"name":"iLIVER","volume":"5 2","pages":"Article 100237"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148186287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay among oncogenic pathways governs hepatobiliary lineage decisions in liver cancer","authors":"Yonglong Pan ,&nbsp;Xiaoping Chen ,&nbsp;Ze-yang Ding","doi":"10.1016/j.iliver.2026.100241","DOIUrl":"10.1016/j.iliver.2026.100241","url":null,"abstract":"","PeriodicalId":100657,"journal":{"name":"iLIVER","volume":"5 2","pages":"Article 100241"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148159656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Medical imaging-derived artificial intelligence for prognostic stratification and treatment response prediction in interventional therapy of hepatocellular carcinoma","authors":"Ying Lei,&nbsp;Tianyi Xia,&nbsp;Yawen Wang,&nbsp;Xinyu Zhou,&nbsp;Xinyu Gao,&nbsp;Shenghong Ju","doi":"10.1016/j.iliver.2026.100240","DOIUrl":"10.1016/j.iliver.2026.100240","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is a malignant tumor that is common worldwide. It is characterized by high incidence and mortality rates. Interventional therapy is a minimally invasive treatment for HCC that offers diverse methods that cover different stages. Because of the significant heterogeneity of tumors, even at the same stage, the effectiveness of interventional therapy can vary greatly, which makes it difficult for clinicians to determine the optimal treatment plan before treatment. Increasing evidence suggests that tumor-related imaging characteristics are correlated with biological functions and can be used to predict different subtypes of HCC and reflect their heterogeneity. In recent years, artificial intelligence (AI) has received widespread attention and been applied widely. AI can automatically extract features from medical images, objectively quantifying low-dimensional to high-dimensional information about tumors, which helps to directly or indirectly predict prognostic stratification and treatment response to interventional therapy. Furthermore, when AI integrates high-dimensional quantifiable information from imaging data with multimodal clinical and molecular data, its accuracy and interpretability improve significantly. Although image-derived AI models have achieved good performance and have broad prospects for application in the prognosis and treatment of HCC, their clinical implementation has limitations, including data and imaging standardization, model interpretability, and the need for multicenter validation. This review summarizes the latest advancements in medical image-driven AI in the prognostic stratification and efficacy prediction of interventional therapy for HCC, and outlines the main challenges that need to be addressed and good prospects for application.</div></div>","PeriodicalId":100657,"journal":{"name":"iLIVER","volume":"5 2","pages":"Article 100240"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148186288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological aging across the metabolic dysfunction–associated steatotic liver disease spectrum: A systematic review","authors":"Chukwuemeka E. Ogbu ,&nbsp;Stella C. Ogbu ,&nbsp;Chidera P. Ogbu ,&nbsp;Chinazor Umerah","doi":"10.1016/j.iliver.2026.100222","DOIUrl":"10.1016/j.iliver.2026.100222","url":null,"abstract":"<div><h3>Background and aims</h3><div>Metabolic dysfunction–associated steatotic liver disease (MASLD) is a growing global health burden. Geroscience posits that accelerated biological aging is a key driver of chronic disease. We systematically reviewed the evidence to define the role of biological aging (BA) across the MASLD disease spectrum.</div></div><div><h3>Methods</h3><div>A systematic literature search of PubMed/MEDLINE and Embase was conducted from inception through August 2025 for observational studies in adults assessing validated BA measures (phenotypic age, Klemera–Doubal method, Homeostatic Dysregulation, epigenetic clocks, telomere length) and MASLD outcomes. A narrative synthesis was performed following SWiM guidelines because of substantial methodological heterogeneity.</div></div><div><h3>Results</h3><div>Nineteen studies were included. BA was operationalized using clinical composite clocks (KDM-BA, PhenoAge, Homeostatic Dysregulation), epigenetic clocks, leukocyte telomere length, homeostatic dysregulation indices, and one machine-learning BA metric. Accelerated BA generally referred to BA higher than expected for chronological age or shorter telomere length. Across large cross-sectional studies, individuals with accelerated BA had higher odds of MASLD/nonalcoholic fatty liver disease (NAFLD), and in prospective cohorts, higher BA at baseline predicted increased hazards of incident NAFLD after multivariable adjustment, suggesting BA functions as an upstream integrator of risk rather than only a consequence of liver disease. Accelerated BA was also associated with greater fibrosis burden and with higher all-cause mortality among people with MASLD. Several studies indicated that BA mediates part of the effect of environmental toxicants on MASLD and acts as an effect modifier, with higher risk observed when accelerated BA co-occurs with unfavorable genetic profiles or environmental exposures. Mendelian randomization analyses supported a potential causal role of cellular aging in liver fibrogenesis.</div></div><div><h3>Conclusion</h3><div>Across 19 observational studies, accelerated biological aging (assessed using clinical composite indices, epigenetic clocks, and telomere length) was consistently associated with higher MASLD/NAFLD risk, greater fibrosis severity, and higher mortality. These findings support BA as potentially a clinically relevant risk integrator in MASLD spectrum diseases. However, heterogeneity in BA measures and disease definitions limits comparability and highlight the need for harmonized BA measures in longitudinal studies.</div></div>","PeriodicalId":100657,"journal":{"name":"iLIVER","volume":"5 1","pages":"Article 100222"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147313899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a hybrid deep learning-based framework for liver fibrosis classification using ultrasound images","authors":"Adedotun F. Adesina ,&nbsp;Blessing O. Olorunfemi ,&nbsp;Adenike T. Adeniji-Sofoluwe ,&nbsp;Chiagoziem A. Otuechere ,&nbsp;Funmilayo Olopade ,&nbsp;Benjamin Aribisala","doi":"10.1016/j.iliver.2026.100225","DOIUrl":"10.1016/j.iliver.2026.100225","url":null,"abstract":"<div><h3>Background and aims</h3><div>Liver fibrosis is a progressive accumulation of extracellular matrix proteins with distortion of hepatic architecture and can progress to cirrhosis or hepatocellular carcinoma. Biopsy remains the diagnostic gold standard, however, its invasive nature, sampling error, and cost limit routine use. Ultrasound imaging provides a safer, more accessible option but depends on operator expertise and subjective interpretation. Existing deep learning approaches for fibrosis assessment often rely on small datasets or perform only binary classification. This study aimed to develop a hybrid deep learning model combining ResNet50 and VGG16 for automated multi-class classification (F0–F4), enhancing diagnostic accuracy, reducing biopsy reliance, and supporting affordable, interpretable liver disease assessment.</div></div><div><h3>Methods</h3><div>The total of 6323 ultrasound image samples with METAVIR system labels ranging from F0 to F4 was downloaded from Kaggle. After data preprocessing, 80:20 splits were made for training and testing. A hybrid model consisting of fine-tuned ResNet50 and VGG16 was used for classification of fibrosis stages. Model performance was statistically evaluated using sensitivity, specificity, and area under the ROC curve (AUC) for each fibrosis stage, averaging across classes to address imbalance. Robustness and reproducibility were assessed by calculating 95% confidence intervals (CI) for all performance metrics through bootstrap resampling. Grad-CAM was used to interpret the model’s predictions.</div></div><div><h3>Results</h3><div>The hybrid model was also successful in achieving the highest peak in testing accuracy, reaching 86.64%, compared to the other models (55.26% for ResNet50, 72.73% for VGG16). The classification was also high for the hybrid model, with the highest values for the macro AUC and weighted AUC at 96.79% and 97.79%, respectively. The highest predicted probabilities were seen for the F0 and F4 stages, which were correctly classified, with the Grad-CAM heatmaps showing high focus on the fibrotic regions.</div></div><div><h3>Conclusion</h3><div>The hybrid model achieved good diagnostic results with high sensitivity, specificity, and confidence. The Grad-CAM images validated that the model was focusing on significant areas, as shown by the heat map, which proves that it has potential as a non-invasive, accurate, and interpretable tool for automated liver fibrosis staging using ultrasound images.</div></div>","PeriodicalId":100657,"journal":{"name":"iLIVER","volume":"5 1","pages":"Article 100225"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147313947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-port robot-assisted hepatectomy of segments S4b and S5v: A case report","authors":"Xin Lan,&nbsp;Jian Feng,&nbsp;Chenglin Piao,&nbsp;Qiang Li,&nbsp;Zhenduo Si,&nbsp;Chao Zhang,&nbsp;Jianjun Leng","doi":"10.1016/j.iliver.2026.100223","DOIUrl":"10.1016/j.iliver.2026.100223","url":null,"abstract":"<div><div>We report a 63-year-old man with hepatocellular carcinoma who initially underwent transcatheter arterial chemoembolization and two cycles of targeted therapy combined with immunotherapy, which achieved a partial response. He then successfully underwent single-port robot-assisted resection of liver segments S4b and S5v using the SHURUI single-port robotic system. The surgical incision measured 4 cm, intraoperative blood loss was 200 mL, and the operation time was 240 minutes. He recovered well and was discharged on postoperative day 7.</div></div>","PeriodicalId":100657,"journal":{"name":"iLIVER","volume":"5 1","pages":"Article 100223"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146189862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}