While metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with obesity, the cause of its rapidly rising prevalence is not well understood. In this study, we aimed to examine the association between arsenic exposure and MASLD in humans.

Urinary inorganic arsenic data from the National Health and Nutrition Examination Survey, 2011–2020, were used. These were combined with death certificate data from the National Death Index of the National Center for Health Statistics to ascertain mortality rates. Weighted linear regression and chi-squared analysis were performed.

The analysis included 6,386 participants after exclusions. The mean urinary arsenic level was 5.92 µg/L in participants with MASLD versus 5.59 µg/L in those without. Alanine aminotransferase levels exhibited a statistically significant increasing trend across both continuous arsenic levels and arsenic quintiles. A statistically significant upward trend was observed for the income-to-poverty ratio and body mass index but not for education status. MASLD prevalence was highest among the white population, while an increasing trend was observed in the Hispanic population over the years (p < 0.001). The proportion of Mexican Americans increased to 12.6% in the MASLD group versus 8.09% in the non-MASLD cohort (p < 0.001). There was a statistically significant increase in the odds of MASLD across arsenic exposure levels, with individuals in the highest quintile having a 32% greater likelihood compared to those in the lowest quintile (p-trend = 0.002). The odds further increased to 55% in the highest quintile (odds ratio 1.55, 95% confidence interval: 1.19–2.03; p-trend < 0.001). MASLD was more prevalent in females than males (57.9% vs. 47.6%; p < 0.001), and the mean age increased from 46.9 years to 49.9 years (p = 0.016).

Our findings reveal a positive association between urinary arsenic exposure and MASLD, with increasing trends particularly observed among Hispanics and those with higher income-to-poverty ratios and body mass index.

Given the high burden of hepatocellular carcinoma (HCC), risk stratification in patients with cirrhosis is critical but remains inadequate. In this study, we aimed to develop and validate an HCC prediction model by integrating radiomics and deep learning features from liver and spleen computed tomography (CT) images into the established age-male-ALBI-platelet (aMAP) clinical model.

Patients were enrolled between 2018 and 2023 from a Chinese multicenter, prospective, observational cirrhosis cohort, all of whom underwent 3-phase contrast-enhanced abdominal CT scans at enrollment. The aMAP clinical score was calculated, and radiomic (PyRadiomics) and deep learning (ResNet-18) features were extracted from liver and spleen regions of interest. Feature selection was performed using the least absolute shrinkage and selection operator.

Among 2,411 patients (median follow-up: 42.7 months [IQR: 32.9–54.1]), 118 developed HCC (three-year cumulative incidence: 3.59%). Chronic hepatitis B virus infection was the main etiology, accounting for 91.5% of cases. The aMAP-CT model, which incorporates CT signatures, significantly outperformed existing models (area under the receiver-operating characteristic curve: 0.809–0.869 in three cohorts). It stratified patients into high-risk (three-year HCC incidence: 26.3%) and low-risk (1.7%) groups. Stepwise application (aMAP → aMAP-CT) further refined stratification (three-year incidences: 1.8% [93.0% of the cohort] vs. 27.2% [7.0%]).

The aMAP-CT model improves HCC risk prediction by integrating CT-based liver and spleen signatures, enabling precise identification of high-risk cirrhosis patients. This approach personalizes surveillance strategies, potentially facilitating earlier detection and improved outcomes.

Imbalanced autonomic function has been reported in gastrointestinal (GI) disorders. The vagus nerve is a major component in the regulation of upper GI motility. Vagal nerve stimulation (VNS) has been shown to improve symptoms of various GI disorders by enhancing parasympathetic activity. This review aims to summarize the clinical efficacy of transcutaneous VNS for GI disorders, focusing on abdominal pain, other GI symptoms, and GI motility, and to discuss the mechanisms of action of transcutaneous VNS. Randomized clinical trials investigating transcutaneous VNS in several major GI disorders, including functional dyspepsia, gastroparesis, constipation, irritable bowel syndrome, and inflammatory bowel disease, were reviewed and discussed. The forms of transcutaneous VNS covered in this review include transcutaneous auricular VNS, transcutaneous cervical VNS, and percutaneous electrical nerve field stimulation. Transcutaneous VNS has been shown to relieve abdominal pain, improve GI symptoms, and accelerate GI motility by enhancing vagal activity in patients with various GI disorders. Transcutaneous VNS is an innovative, effective, and safe therapy for patients with GI disorders; however, large-scale clinical trials are necessary to establish optimal treatment modalities and efficacy.

Glioblastoma (GBM) is the most prevalent and aggressive form of primary brain malignancy in adults. Despite continuous advancements in standard treatment modalities, the prognosis for patients remains extremely poor, with a median survival of less than two years. In recent years, chimeric antigen receptor T-cell (CAR-T) therapy has achieved revolutionary success in hematologic malignancies, marking a significant breakthrough in the field of immunotherapy. However, the successful application of CAR-T therapy to GBM still faces dual challenges: antigen heterogeneity and the immunosuppressive tumor microenvironment. This review systematically summarizes these challenges encountered in CAR-T therapy for GBM and the innovative strategies currently under development to address these challenges, providing insights for the future clinical translation of CAR-T therapy in GBM.

Actively identifying the risk factors and predictive indicators associated with portal vein thrombosis (PVT) in liver cirrhosis (LC) can enable early diagnosis and treatment, which is of great significance for prolonging the survival of patients with LC. Hemodynamic disturbances, advanced LC, vascular endothelial injury, and mutations in thrombophilic genetic factors are established risk factors for PVT-LC. Venous dilatation and decreased blood flow velocity contribute to hemodynamic disturbances. The severity of LC can be assessed by the degree of portal hypertension, liver metabolic function biomarkers, and validated liver scoring systems. Iatrogenic interventions, endotoxemia, and metabolic syndrome may induce vascular endothelial injury and hypercoagulability, the latter of which can be quantified via coagulation-anticoagulation-fibrinolysis biomarkers. Mutations in thrombophilic genetic factors, such as Factor V Leiden, MTHFR C667T, and JAK2 V617F, disrupt coagulation-anticoagulation homeostasis and predispose patients to PVT-LC. This review specifically focuses on comprehensively delineating established risk factors and predictive indicators for PVT-LC, thereby providing a theoretical foundation for the construction of clinically applicable PVT predictive models to guide early interventions and improve the prognosis. Future research should further validate the associations between recently proposed risk factors and PVT-LC, while simultaneously establishing cutoff values for indicators with robust predictive value to construct a clinically applicable PVT prediction framework.

Giant invasive spinal schwannoma (GISS) is a rare benign tumor that extends over two or more vertebral levels with myofascial invasion. No previous case of GISS with vertebral body collapse has been reported. A 44-year-old man presented with a one-year history of progressive limb weakness and difficulty with defecation. He was initially misdiagnosed with a metastatic spinal tumor. Imaging revealed a large extradural mass with C4 vertebral body collapse. Histological examination of tumor tissue from both operations confirmed the diagnosis of schwannoma. The postoperative course was uneventful, and the patient’s limb weakness gradually improved. One year after surgery, the patient was able to walk and write independently. Muscle strength recovered to 4/5 in the upper extremities and 5/5 in the lower extremities, with a modified Japanese Orthopaedic Association score of 15/15. The patient’s neurological function improved significantly, and one-year follow-up showed no recurrence and stable spinal fixation. Currently, the patient’s bowel function has improved; however, the patient still requires defecation in bed. When magnetic resonance imaging reveals giant spinal tumors with imaging features suggestive of malignancy, GISS should be considered. Preoperative biopsy is essential for accurate diagnosis.

Achalasia is a motility disorder of the esophagus, characterized by failure of relaxation of the lower esophageal sphincter and disordered peristalsis. Although it is a rare condition, its incidence is rising, likely due to advances in diagnostic techniques and the adoption of standardized definitions. Achalasia is associated with significant morbidity, and currently, there is no cure. Pharmacologic, endoscopic, and surgical interventions are aimed at symptom control. Laparoscopic Heller myotomy (LHM) has been the standard of care for achalasia since the 1990s. Over the past two decades, per-oral endoscopic myotomy (POEM) has emerged as a viable treatment option. Today, LHM and POEM represent the two most effective treatment modalities available for achalasia. This review aims to compare outcomes following LHM and POEM for achalasia and to explore patient characteristics and technical factors that guide optimal treatment selection. We examine the evidence regarding dysphagia relief, reflux, complications, and reintervention rates for both procedures, taking into account factors such as prior surgical history, achalasia subtype, and patient comorbidities.

Chronic hepatitis B virus (HBV) infection remains a major cause of liver diseases, including cirrhosis and hepatocellular carcinoma. Reliable biomarkers for assessing viral replication, liver damage, and predicting clinical outcomes are essential for effective patient management. This review focuses on two promising biomarkers: serum HBV RNA and hepatitis B core-related antigen, both of which show strong correlations with viral replication and disease progression. Serum HBV RNA levels reflect the quantity and transcriptional activity of intrahepatic covalently closed circular DNA, providing insights into viral replication. They also correlate with other markers of replicative activity and have predictive value for key clinical outcomes, including hepatitis B e antigen and hepatitis B surface antigen seroconversion, relapse after therapy cessation, and liver fibrosis. Similarly, hepatitis B core-related antigen is closely associated with covalently closed circular DNA levels, correlates with markers of viral replication, and shows promise in predicting liver fibrosis, cirrhosis, and the risk of hepatocellular carcinoma. This review highlights the potential of both biomarkers for monitoring disease progression and guiding therapeutic decisions, particularly in the context of personalized treatment strategies and risk assessment for liver-related complications.

Acetaminophen (APAP) is one of the most commonly used analgesic and antipyretic medications and is generally considered safe at therapeutic doses. However, overdose remains a leading cause of acute liver failure, primarily characterized by centrilobular (zone 3) hepatic necrosis, oxidative stress, mitochondrial dysfunction, and sterile inflammation. The hepatotoxic effects of APAP are localized to the centrilobular region, where cytochrome P450 2E1 is highly expressed. Cytochrome P450 2E1 catalyzes the conversion of APAP to a toxic metabolite, N-acetyl-p-benzoquinone imine. During overdose, the liver’s detoxification capacity is overwhelmed and excess N-acetyl-p-benzoquinone imine binds to cellular proteins, initiating oxidative stress and mitochondrial injury that culminate in hepatocyte death. A central component of APAP-induced hepatotoxicity is the activation of innate immune responses, particularly via inflammasome pathways. Inflammasomes are cytosolic multiprotein complexes that detect cellular damage and trigger inflammation. Among these, the NOD-, LRR-, and pyrin domain-containing 3 (NLRP3) inflammasome plays a significant role in APAP-induced liver injury. Upon activation, the NLRP3 inflammasome promotes autocatalytic cleavage of procaspase-1 into its active form, caspase-1, which subsequently processes the pro-inflammatory cytokines pro-interleukin-1β and pro-interleukin-18 into their mature forms. These cytokines recruit additional immune cells and amplify liver inflammation, exacerbating tissue injury. Thus, the NLRP3 inflammasome serves as a key mechanistic link between the initial toxic insult and the ensuing inflammatory response in APAP hepatotoxicity. This review aimed to explore the molecular mechanisms underlying APAP-induced liver injury, particularly inflammasome activation, and evaluate the current and emerging therapeutic strategies.