Autosomal dominant acute porphyrias are rare inherited disorders of haem biosynthesis characterised by accumulation of potentially neurotoxic porphyrin precursors and attacks of severe abdominal pain with autonomic and neuropsychiatric features. Disease severity ranges from asymptomatic individuals to those with recurrent, life-threatening attacks. The International Porphyria Network invited 34 acute porphyria specialists from 17 countries to form an expert panel. The invited group included clinicians from diverse specialities (ie, internal medicine, haematology, endocrinology, gastroenterology, hepatology, neurology, and biochemistry), together with laboratory scientists and patient representatives. The panel met online (in 2023-25) to develop 15 evidence-based recommendations with the use of the Grading of Recommendations, Assessment, Development, and Evaluations framework addressing attack prevention, management of sporadic and recurrent attacks, long-term follow-up, surveillance for primary liver cancer, and family screening. The guidelines support safe, consistent clinical care and improved outcomes, recognising global variation in resources and access to high-cost drugs, and highlighting priorities for future research.
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The heterogeneity of ulcerative colitis (UC) results in variable biological responses. Although anti-tumor necrosis factor (anti-TNF) agents remain a cornerstone of therapy, 30-40% of patients experience primary non-response, which is often linked to persistent activation of the interleukin-23 (IL-23) pathway. There is increasing evidence that the IL-23-Th17-neutrophil axis plays a central role in mucosal inflammation and treatment resistance. Phase II and III trials of selective IL-23 inhibitors for UC have demonstrated high rates of endoscopic and histologic remission, with safety profiles comparable to those of anti-TNF agents. These agents have demonstrated efficacy in various patient subgroups, including those with a history of anti-TNF failure. This supports their potential as effective alternatives to existing biologics. Based on these data, we propose a multimodal framework for personalized treatment selection that integrates three diagnostic pillars: (1) noninvasive biomarkers, such as serum leucine-rich alpha-2 glycoprotein and fecal calprotectin, to differentiate between systemic and mucosal inflammation, (2) the Mayo Endoscopic Subscore to guide therapeutic intensity, and (3) quantitative histopathology, specifically the Komagane subclassification of Geboes Grade 3, to identify IL-23-Th17-dominant activity. This integrative approach may enable predicting biologic responses, risk stratification, and the individualized use of selective IL-23 inhibitors. We propose this strategy as a model for generating hypotheses for future personalized medicine studies in UC.
This study aimed to investigate the relationship between admission serum lipase levels, prognostic clinical scoring systems, and in-hospital mortality in patients presenting to the emergency department with acute pancreatitis. This retrospective cohort study included 389 patients hospitalized with acute pancreatitis at a tertiary care center between 2021 and 2023. Demographic characteristics, clinical findings, laboratory parameters obtained at admission and at 48 h, and imaging findings were collected. Prognostic assessment was performed using the Ranson, APACHE II, BISAP, Glasgow-Imrie, HAPS, and CTSI scoring systems. Patients were categorized according to a predefined serum lipase cutoff of 600 U/L. The associations between serum lipase levels, prognostic score categories, and in-hospital mortality were analyzed, and the diagnostic performance of the lipase cutoff was evaluated. The overall in-hospital mortality rate was 3.9% (n = 15). Admission serum lipase levels were significantly associated with the Ranson score (p < 0.05) and several laboratory parameters. A serum lipase cutoff of 600 U/L identified patients with a Ranson score ≥ 3 with a sensitivity of 70.2% (95% CI: 60.4-78.8) and a specificity of 57.3% (95% CI: 51.2-63.2). Higher prognostic scores, including Ranson, BISAP, and APACHE II, were significantly associated with in-hospital mortality (p < 0.01). However, admission serum lipase levels were not significantly associated with in-hospital mortality. Admission serum lipase showed a limited association with selected prognostic indicators in acute pancreatitis but was not associated with in-hospital mortality. These findings suggest that serum lipase has limited value as a standalone prognostic marker and should be interpreted in conjunction with established clinical scoring systems. Further prospective studies are needed to better clarify its role in risk assessment.
The gut microbiota plays a pivotal role in bio-transforming dietary components, including tryptophan, an essential amino acid that undergoes microbial metabolism. Microbial metabolism of tryptophan yields indole-3-propionic acid (IPA), an emerging biomarker for gut inflammation. Current IPA detection relies on expensive, time-consuming mass spectrometry. To address this limitation, a fluorescent nanosensor system is presented that uniquely features two optical modalities: one utilizing near-infrared (NIR) emission of a central single-walled carbon nanotube (SWNT), and a separate, visible emission from the corona phase polymer, a cationic conjugated polyelectrolyte (CP3). Selective IPA molecular recognition occurs at the latter, but the binding is optically reported via quenching in both the visible and NIR emission channels. The two modalities provide complementary advantages: CP3-SWNTs' NIR channel enables detection in strongly scattering tissue environments due to reduced Rayleigh scattering at longer wavelengths. Conversely, CP3 visible channel facilitates future rapid, cost-effective point-of-care biological sample screening. Functionality of both modalities is maintained within a gelatin metacrylate hydrogel offering potential for future continuous in vivo monitoring of IPA dynamics. The sensor reveals significant differences in plasma IPA levels between healthy controls and patients with active gut inflammation: ulcerative colitis and Crohn's disease, highlighting its promise in rapid gut health assessment.
Two-dimensional shear wave elastography (2D-SWE) is a non-invasive technique for assessing liver fibrosis. However, its clinical utility has not been fully established. This study evaluated the diagnostic accuracy of 2D-SWE using magnetic resonance elastography (MRE) as the reference standard in a retrospective, multicenter, large-scale cohort. A total of 744 patients with chronic liver disease were included in the analysis. The association between 2D-SWE measurements and fibrosis stages determined by MRE was assessed. The correlation between 2D-SWE and MRE values was analyzed, and the diagnostic performance of 2D-SWE was evaluated using receiver operating characteristic (ROC) curve analysis. As 2D-SWE and MRE values were not normally distributed, they were log-transformed (Log-2D-SWE and Log-MRE) for analysis. A strong correlation was observed between Log-2D-SWE and Log-MRE values, with a correlation coefficient of 0.764 (p < 0.001). When 2D-SWE values were stratified according to the histological stages of liver fibrosis (F0-F4), based on MRE data, the corresponding median values were 4.61, 5.63, 6.18, 7.44, and 11.64 kPa, respectively (p < 0.001, Jonckheere-Terpstra test). The areas under the ROC curve (AUROCs) and cutoff values for 2D-SWE were 0.872 and 5.47 kPa for ≥ F1 (n = 285), 0.894 and 5.88 kPa for ≥ F2 (n = 217), 0.931 and 6.48 kPa for ≥ F3 (n = 137), and 0.937 and 7.39 kPa for F4 (n = 81), respectively. In subgroup analyses, AUROCs for detecting ≥ F2, ≥F3, and F4 exceeded 0.78, even among patients with elevated body mass index or advanced hepatic steatosis. 2D-SWE represents a highly useful and reliable non-invasive modality for assessing of liver fibrosis.
Duodenal tumors constitute 35%-55% of small bowel neoplasms, yet the misdiagnosis rate remains substantial. This study investigated the clinical features of duodenal tumors missed during endoscopic examination. This retrospective cohort analysis included patients who were diagnosed with duodenal tumors between 2019 and 2023 at West China Hospital. Demographic data, tumor characteristics, endoscopic findings, and missed diagnosis records were extracted from electronic medical records and telephone follow-ups. The exploratory analysis identified the reasons for the missed diagnosis during endoscopy. Among the 307 enrolled patients with duodenal tumors, 36 patients (34 with adenocarcinomas and 2 with neuroendocrine tumors) had undergone previous endoscopic examinations without a definitive diagnosis, yielding a missed detection rate of 11.7%. In all missed cases, the mean number of endoscopic procedures performed prior to definitive diagnosis was 2 (range: 1-8), with an average interval of 11.1 months (range: 3-36 months). The anatomical distribution of missed lesions included the duodenal papilla (44.4%, 16/36), duodenal bulb (25.0%, 9/36), bulb-descending junction (5.6%, 2/36), descending (13.9%, 5/36) and horizontal (5.6%, 2/36) parts. The causes of missed diagnoses included exposure errors (n = 20), judgment errors (n = 5), biopsy errors (n = 8), and unclassified errors (n = 3). The difference in the pattern of missed duodenal tumors between tertiary hospitals and non-tertiary hospitals was not statistically significant (P > 0.05). The missed diagnosis rate of duodenal tumors is high during endoscopic examination. Comprehensive endoscopic observation and improved detection awareness of duodenal tumors are essential in both tertiary and nontertiary hospitals.
Wilson disease (WD) is a rare autosomal recessive disorder of copper metabolism presenting with acute liver failure, cirrhosis, or neurologic involvement. Liver transplantation (LT) is the definitive treatment; however, data remain limited, particularly from regions reliant on living donor LT (LDLT). We retrospectively analyzed a prospectively collected transplant database, identifying all patients (≥ 14 years) who underwent LT for WD between January 2001 and December 2023. Data on demographics, LT indications, disease characteristics, pre-transplant therapy, complications, and outcomes were collected. Survival was assessed using Kaplan-Meier methods, and neurologic outcomes from clinical documentation. Forty-one patients underwent LT for WD (median age: 23 years; 51.2% female). Ascites was present in 68.4%, encephalopathy in 32.4%, and hepatocellular carcinoma in 5.1%. Acute liver failure was the initial presentation in 17.9%. LDLT comprised 53.7%. Acute cellular rejection occurred in 29.7% but was manageable; no patient required re-transplantation. Neurologic involvement was present in 17.1%, with 71% improving post-LT. One-, five-, and ten-year survival rates were 94%, 94%, and 82%. LT for WD yields excellent long-term survival. Neurologic improvement occurred in most Neuro-Wilson patients, supporting LT even in neurologically affected cases. LDLT plays a crucial role in regions with limited deceased donors.
Alterations of the gut microbiome have been reported in central nervous system demyelinating diseases. While the gut microbiome in pediatric multiple sclerosis (MS) has been studied, the role of the gut microbiome in other pediatric-onset acquired demyelinating syndromes (ADS) remains unknown. We compared the gut microbiome composition between myelin oligodendrocyte glycoprotein antibody-positive (MOG+) and antibody-negative (MOG-) participants with pediatric-onset ADS. Participants aged ≤21 years enrolled in the Canadian Pediatric Demyelinating Disease Network microbiome study (2015-2018) with a single episode or relapsing non-MS, non-neuromyelitis optica spectrum disease attacks of demyelination with symptom onset <18 years were included. Stool sample-derived DNA underwent 16S rRNA (V4) sequencing. Serum MOG-IgG antibodies were tested within 30 days of first attack onset. Alpha-diversity (Shannon, Margalef's index, Chao1) and beta-diversity (weighted UniFrac) were analysed. Phylum/genus-level taxa were assessed using negative binomial models with false discovery rate correction. Rate ratios were sex- and age-adjusted (aRR). Forty-six participants (18 MOG+/28 MOG-) were included. Mean age at stool sample collection (MOG+/MOG-) was 14.7/17.2 years. Alpha-/beta-diversities did not differ between MOG+/MOG- participants (p > 0.3). At the phylum level, the relative abundance of Proteobacteria was lower in MOG+ than MOG- participants (aRR:0.22;95%CI:0.07-0.69;q = 0.03). At the genus level, the relative abundance of Escherichia/Shigella was lower in MOG+ than MOG- participants (aRR:0.01;95%CI:0.001-0.07;q = 0.001), CONCLUSIONS: While alpha/beta-diversities did not differ between MOG+/MOG- participants, taxa-level differences were observed. Our findings suggest that the gut microbiome composition may differ by MOG serostatus among pediatric-onset ADS participants. Future work is warranted, utilizing larger cohorts and longitudinal follow-up.
Gastric diseases are a major health burden, especially in East Asia, with high incidence and mortality rates. While Helicobacter pylori infection and poor lifestyle behaviors are established risk factors, the impact of drug-related gastric injury in aging populations remains underexplored. In China, polypharmacy is common among older adults, with nearly 40% using self-purchased medications without professional guidance. Similar trends are observed in other aging societies, highlighting the global challenge of unregulated drug use. Existing studies lack adjustments for comorbidities, prediction tools, and methodological innovation. This study analyzes CHARLS 2018 data to: (1) examine the relationship between self-purchased medication use and gastric disease, and (2) identified strongly associated groups, such as patients with chronic kidney disease (CKD) and diabetes. We included 19,752 participants from the CHARLS database. Participants were divided into gastric disease and control groups based on DA007_10 questionnaires. We compared baseline characteristics, including self-purchased medication use, between groups. Multivariate logistic regression models were used to assess the correlation between self-purchased medication use and gastric disease. The receiver operating characteristic (ROC) curve evaluated Model 3's predictive performance. Stratified analysis was conducted to assess the stability of the results. Significant differences were observed between the gastric disease (n = 659) and control (n = 5,428) groups in factors such as ethnicity, self-reported health status, hypertension, dyslipidemia, diabetes, chronic lung diseases, liver disease, kidney disease, smoking history, and medication use. In all models, self-purchasing medication was associated with an increased prevalence of gastric disease (adjusted OR = 1.75, 95% CI 1.46-2.09, p < 0.001), including Model 3 (adjusted OR = 1.75, 95% CI 1.46-2.09, p < 0.001). The model demonstrated moderate discriminatory ability in distinguishing individuals with and without gastric disease (AUC = 0.71). Stratified analyses revealed that the association between self-purchased medication use and gastric disease risk was consistent across covariates, with stronger effects observed in participants with CKD (adjusted OR = 1.89) and diabetes (OR = 1.82). This study found that self-purchasing medication was positively correlated with the risk of gastric disease in Chinese older adults (adjusted OR = 1.75), and the association was stronger among those with chronic kidney disease (adjusted OR = 1.89) or diabetes (OR = 1.82). This finding provides a reference for the risk stratification and prevention strategies of gastric disease.
Endoscopic full-thickness resection (EFTR) for gastric submucosal tumors (SMTs) presents a technical challenge for defect closure. This study aims to evaluate the feasibility and efficacy of a novel mucosal traction-assisted clip closure (MTCC) technique compared to conventional clip closure (CCC). In this multi-center retrospective study of 218 patients undergoing EFTR for gastric SMTs at seven hospitals (June 2020-June 2025), patients were divided into MTCC (n = 32) and CCC (n = 186) groups. To minimize selection bias, 1:2 propensity score matching (PSM) yielded a matched cohort of 96 patients (MTCC, n = 32; CCC, n = 64). Primary outcomes were defect closure success rate and closure time. Secondary outcomes included postoperative complications, fasting time, and hospital stay. Subgroup analyses were performed by defect diameter (≤ 2.5 cm vs. >2.5 cm) and tumor location (gastric fundus). Defect closure was successfully achieved in all patients in the MTCC group. After PSM, baseline characteristics were well-balanced between the two groups. The MTCC group continued to demonstrate superior closure efficiency compared to the CCC group, with a significantly shorter median defect closure time (7.0 min vs. 17.0 min, P < 0.001) and fewer titanium clips used (8.0 vs. 12.0, P < 0.001). The median total procedure time was also significantly reduced in the MTCC group (47.0 min vs. 53.0 min, P = 0.027). Postoperatively, patients in the MTCC group had a shorter median fasting time (2.0 days vs. 3.0 days, P = 0.001), while complication rates remained comparable between groups. The advantages of MTCC were consistently observed across subgroups stratified by defect size and tumor location. After adjusting for potential confounders using PSM, the MTCC technique appears to be a feasible method for managing post-EFTR defects. In this cohort, it was associated with significantly enhanced closure efficiency and accelerated postoperative recovery.
Stathmin-3 (STMN3) is a member of the microtubule-destabilizing regulatory protein family and functions to promote microtubule depolymerization. It specifically binds to the α/β heterodimers of microtubules, facilitating their depolymerization and inhibiting polymerization, thereby influencing cell morphology and function. Recent studies have indicated that aberrant expression of STMN3 is closely associated with the development of various diseases. In the field of oncology, STMN3 has been found to be dysregulated in multiple cancer types and is strongly linked to tumor initiation, progression, and metastasis. Owing to these characteristics, STMN3 is involved in diverse physiological and pathological processes as well as critical signaling pathways, demonstrating its potential as a multifunctional regulatory molecule. This article reviews and analyzes the roles and mechanisms of STMN3 in tumorigenesis, with the aim of identifying potential therapeutic targets and contributing to the development of precision medicine strategies for cancer treatment. This study is a narrative review on the role of STMN3 in tumors, which is guided by the Scale for the Assessment of narrative review articles (SANRA). Literature retrieval was conducted in public databases such as PubMed and Web of Science using "STMN3″, "SCLIP", "tumor", and "cancer" as key words, with no restriction on publication time. Relevant studies were screened based on research content and data integrity, including bioinformatic analyses and in vitro/in vivo experimental studies.
This study aimed to investigate the clinical characteristics and imaging features of walled-off pancreatic necrosis (WOPNs) involving the pancreatic parenchyma in patients with no documented pancreatitis, and to establish a diagnostic prediction nomogram using Lasso regression to differentiate WOPNs from mucinous cystic neoplasms (MCNs). A total of 247 cases were retrospectively collected from three independent hospitals, including surgically confirmed post-inflammatory necrotic collections meeting imaging criteria for WOPNs and pathologically confirmed MCNs. Clinical and imaging features were analyzed, and independent predictors were identified using Lasso regression. Clinical, imaging, and combined diagnostic models were constructed and assessed using ROC, calibration, and decision curve analyses (DCA). A diagnostic nomogram was developed from the best model. Univariate analysis revealed significant differences between WOPNs and MCNs in the training cohort for age, sex, clinical symptoms, lesion location, shape, lesion margin, cyst category, incomplete septation, peripancreatic fat space, density/signal, cyst wall and/or septal thickness, mural nodule, lesion calcification, peripancreatic inflammatory changes, MPD morphology, location of ductal dilation, vascular involvement, and organ involvement (p < 0.05). Lasso regression identified three clinical features, eight imaging features, and five combined clinical and imaging features as independent risk factors, which were subsequently used to construct clinical, imaging, and combined models. The combined model achieved the highest diagnostic performance, with AUC values of 0.880 in the training cohort and 0.858 and 0.856 in the two external validation cohorts, respectively, demonstrating good sensitivity, specificity, and overall accuracy. We established a reliable, non-invasive diagnostic prediction nomogram based on Lasso regression to differentiate WOPNs with no documented pancreatitis from MCNs.
Chronic hepatitis B (CHB) is characterized by progressive structural and functional liver impairment involving hepatic dysfunction, fibrosis accumulation, and nutritional-immune imbalance. Although non-invasive indices derived from routine laboratory parameters-such as the albumin-bilirubin (ALBI) score, fibrosis-4 (FIB-4) index, and prognostic nutritional index (PNI)-are widely used, their integrated value for stage-based risk stratification in HBV-related liver disease remains unclear. To develop and internally validate a clinically applicable, non-invasive risk stratification framework based on ALBI, FIB-4, and PNI, and to evaluate its performance across different clinical stages of HBV-related liver disease. We conducted a single-center retrospective cross-sectional study including 842 hospitalized patients with HBV-related liver disease. Patients were categorized as chronic hepatitis B, compensated cirrhosis, or decompensated cirrhosis at admission. ALBI, FIB-4, and PNI were calculated from routine laboratory data. Ordinal logistic regression was used to identify factors associated with advanced disease stage. Discriminative performance was assessed using receiver operating characteristic (ROC) analysis, and calibration was evaluated. Factors associated with hepatic encephalopathy were explored in patients with decompensated cirrhosis. ALBI and FIB-4 increased with higher disease stage, whereas PNI declined significantly (all P < 0.001). Multivariable analysis identified age, ALBI, and FIB-4 as independent factors associated with advanced stage, while PNI and platelet count were inversely associated. The combined framework was associated with improved discrimination for disease stages compared with individual indices, with further enhancement after incorporation of prothrombin time (PT). Higher ALBI values were independently associated with hepatic encephalopathy among patients with decompensated cirrhosis. An integrated framework combining ALBI, FIB-4, PNI, and PT may provide a simple, interpretable, and cost-accessible tool for stage-based risk stratification in HBV-related liver disease within hospitalized populations.
Accurate detection of KRAS codon mutations is essential for precision oncology in colorectal cancer (CRC), yet conventional liquid biopsy methods often lack sufficient sensitivity for rare ctDNA variants, particularly in early diseases. We developed a three-dimensional (3D) plasmonic KRAS microarray integrating blocked recombinase polymerase amplification with plasmon-enhanced fluorescence. Quencher-modified blocking probes suppress wild-type DNA while selectively enabling mutant signal amplification. A single primer-probe set per codon allows comprehensive detection of all substitutions within KRAS codons 12/13, 61, and 146. The platform achieved detection down to 1 fM by direct hybridization and 100 zM after blocked amplification, exceeding conventional PCR and next-generation sequencing sensitivity. Codon-level specificity was validated in CRC cell lines, with distinct signals for each mutation. Clinical analysis of 58 patients showed 100% concordance between tissue, plasma, and urine in mutation-positive malignant cases when sufficient input was available, indicating accurate reflection of tumor profiles. In benign tumors, detection was rare despite tissue mutations, likely due to limited ctDNA release.This plasmonic microarray enables ultra-sensitive, specific, and non-invasive detection, supporting early diagnosis, minimal residual disease monitoring, and longitudinal CRC management.
Lactate, an energy source and metabolic by-product, has been implicated in cancer progression, but its role in colorectal cancer (CRC) remains incompletely understood. This study investigated the clinical significance, biological effects, and transcriptomic responses of CRC cells to lactate. In human CRC specimens, lactate levels were positively associated with advanced clinical stage and poorer disease-free survival. Functional assays showed that lactate promoted malignant cellular behaviors in both SW480 and HCT116 cells, while pH-control experiments suggested that these effects were not merely due to extracellular acidification alone. RNA sequencing in SW480 cells identified 1,418 differentially expressed genes after lactate treatment. GO and KEGG analyses revealed alterations in multiple metabolic and signaling pathways. qRT-PCR validated the alterations of representative genes, including HK2, VEGFA, JUNB, CCNB1, MAPK4, and COX2. In addition, flow cytometry showed activation of NF-κB and HIF-1α signaling following lactate treatment, and pharmacological inhibition of either pathway significantly attenuated the lactate-induced malignant phenotypes. Together, these findings provide transcriptomic and functional evidence that lactate promotes malignant phenotypes in CRC cells and offer exploratory mechanistic insights into the involvement of NF-κB and HIF-1α signaling.
Seronegative autoimmune hepatitis (SnAIH) lacks detectable conventional autoantibodies (ANA, SMA, anti-LKM, anti-LC1, and anti-SLA/LP), posing diagnostic challenges. Increasing evidence suggests SnAIH in adults reflects limitations in autoantibody detection rather than a distinct variant. We systematically re-evaluated all biopsy-proven SnAIH cases in a large international multicenter AIH cohort using standardized testing. Among 760 patients with baseline liver biopsy, 52 (6.8%) were initially classified as SnAIH. Forty-three lacked complete autoantibody testing, most commonly anti-SLA/LP. After comprehensive re-evaluation, only 9 patients (1.18%) fulfilled criteria for true SnAIH. All presented acutely with markedly elevated transaminases (median ALT 16.1 × ULN); five had elevated IgG levels. Histology suggestive of autoimmune-like drug-induced liver injury was observed in four cases. All but one relapsed after treatment withdrawal, and 42.9% failed to normalize ALT at six months. In conclusion, SnAIH is rare (~1%), highlighting the importance of standardized, comprehensive autoantibody testing and re-testing according to the guidelines.
Artificial intelligence (AI)-assisted endoscopy has been developed for the early detection of upper gastrointestinal cancer; however, its clinical effectiveness remains insufficiently evaluated. This study assessed its effectiveness in a health screening facility. This retrospective cohort study compared AI-assisted and non-AI-assisted upper gastrointestinal endoscopy at Omiya City Clinic, Japan (April 2021-March 2024). Participants who underwent endoscopy between April 2021 and March 2023 were classified as the non-AI group, while those examined between April 2023 and March 2024 comprised the AI group. The AI-assisted system was introduced in April 2023. The primary outcome was cancer detection rate (CDR), with secondary outcomes including biopsy rate and positive predictive value (PPV). Propensity score matching (PSM) was performed for age, sex, alcohol consumption, smoking, Helicobacter pylori infection history, endoscopist experience, and prior-year endoscopy to minimize bias. In total, 17,662 were included in the AI group and 32,318 in the non-AI group. PSM created 17,662 matched pairs. In the AI group, the CDR for gastric cancer (GC) was significantly higher compared to the non-AI group (0.10% vs. 0.03%, p < 0.05). The biopsy rate was slightly higher in the AI group, with no significant difference, whereas the PPV of biopsy for gastric cancer and esophageal cancer was significantly increased (4.84% vs. 2.16%, p < 0.05). In a clinical screening setting, AI-assisted endoscopy significantly improved the CDR of GC and enhanced the PPV of biopsies. These findings highlight AI-assisted endoscopy as a valuable tool for early GC diagnosis in screening environments.
Perivascular epithelioid cell tumors (PEComas) are rare mesenchymal tumors composed of cells exhibiting an epithelioid morphology. These cells typically arrange around small blood vessels (perivascular spaces) and display dual differentiation characteristics of smooth muscle cells and melanocytes. Diagnosis is challenging due to the absence of specific symptoms or tumor markers. This case features a young male patient with a large hepatic PEComa, whose imaging findings resemble those of hepatocellular carcinoma. We have detailed the entire process from diagnosis to treatment to aid in differential diagnosis and surgical planning. A 31-year-old male patient with no prior medical history underwent a routine health examination 20 days prior to presentation. Although the patient was asymptomatic, ultrasound revealed an incidental hepatic lesion measuring 58 × 50 × 45 mm (maximum diameter 58 mm, or 5.8 cm). The screening center suspected a hemangioma. Subsequently, he presented to our hospital. Comprehensive imaging studies, including ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI), revealed a 58 mm-diameter space-occupying lesion in segments V and VIII of the right hepatic lobe. Imaging findings initially raised suspicion for hepatocellular carcinoma. To minimize surgical trauma and preserve liver function, our team discussed surgical approaches and ultimately decided on a laparoscopic partial hepatectomy. During the procedure, we obtained a specimen for pathological examination. The final histopathological analysis confirmed the diagnosis of a PEComa with undetermined malignant potential. The patient recovered smoothly postoperatively and was successfully discharged. PEComa has an insidious onset and is rare. Early diagnosis is often challenging, and imaging studies typically show no highly specific findings. Clinical diagnosis frequently relies on biopsy. In terms of treatment, radical resection (R0 resection, i.e., negative margins) represents the definitive therapeutic approach.
Human liver tissue-derived organoids recapitulate key hepatic phenotypes but are commonly maintained under static conditions, whereas microfluidic organ-on-chip systems provide controllable perfusion and mass transport. Scalable integration of human liver tissue-derived organoids into a perfused, human-relevant Liver-on-Chip remains limited. We combined healthy human liver tissue-derived organoids with a high-throughput three-lane OrganoPlate microfluidic format to establish a perfused organoid Liver-on-Chip (HepLoC) featuring 3D luminal tubules under continuous flow. After hepatocyte-directed differentiation under perfusion, bioengineered HepLoC formed mature hepatocyte-like architectures with increased mature hepatocyte marker proteins, enrichment of hepatic transcriptomic signatures, and functional bile canaliculi. As a proof-of-concept for drug-induced liver injury, troglitazone induced dose-dependent hepatocyte injury accompanied by tight-junction disruption, MRP2 mislocalization, and impaired bile acid export, recapitulating key features of cholestatic liver injury. To model metabolic liver disease, free fatty acids triggered lipid droplet accumulation, increased triglycerides and reactive oxygen species, and upregulated lipogenic and inflammatory genes while largely preserving viability, consistent with early-stage metabolic dysfunction-associated fatty liver disease. The high-throughput HepLoC format further enabled parallel testing of reference hepatotoxic drugs and curcumin liposomes by reduced lipid accumulation in fatty-acid-treated HepLoC with minimal hepatotoxicity. Our perfused, organoid-based microfluidic Liver-on-Chip recapitulates essential human liver structure and function and enables integrated, parallel evaluation of hepatotoxicity and optimization of nanotherapeutic strategies, which deciphers the mechanisms of liver diseases, bridging the gap between preclinical research and clinical translation.