Autoimmune hepatitis (AIH) is a severe immune-mediated liver disease with limited treatment options beyond immunosuppressants, which carry significant side effects. Existing evidence suggests that mesaconate (MSA) possesses immunomodulatory properties and may offer advantages over itaconate derivatives by avoiding succinate dehydrogenase inhibition. However, its specific role in AIH remains unclear. This study aimed to investigate the therapeutic effects of MSA on AIH and to elucidate its underlying mechanisms of action.

A murine AIH model was established via tail vein injection of concanavalin A (ConA, 20 mg/kg). MSA (250 mg/kg) was administered intraperitoneally 6 h before ConA exposure. Liver histology, serum transaminase levels, apoptosis markers, oxidative stress markers, and inflammatory cytokines were analyzed to assess the therapeutic efficacy of MSA. Additionally, RNA sequencing and Western blotting were performed to explore the mechanisms of MSA action. In vitro validation was conducted using RAW264.7 macrophages pretreated with MSA (1 mM) followed by interferon-gamma (IFN-γ, 50 ng/mL) stimulation.

MSA pretreatment effectively mitigated ConA-induced AIH by reducing inflammatory responses, oxidative stress, and apoptosis both in vivo and in vitro. The underlying protective mechanism involved MSA-mediated downregulation of IFN-γ expression and subsequent inhibition of the Janus tyrosine kinase 1/2–signal transducer and activator of transcription 1 signaling pathway. The involvement of this pathway in human AIH was also confirmed.

This study provides the first evidence that MSA ameliorates AIH by suppressing the IFN-γ–Janus tyrosine kinase 1/2–signal transducer and activator of transcription 1 signaling pathway, offering novel mechanistic insights and a promising therapeutic candidate for the future treatment of autoimmune disorders.

Terminal ileum intubation is considered the completion step of colonoscopy and is usually performed to assess the ileum. The histological examination of the ileal mucosa, which is acquired during terminal ileum intubation, may allow an accurate diagnosis. However, there is no absolute consensus on when ileoscopy and biopsy should be attempted. As a result, we aimed to evaluate whether terminal ileum intubation and biopsy should be performed routinely.

Systematic searches were performed in the PubMed, EMBASE, and Cochrane Library databases, as well as the Science Citation Index via the Web of Science platform. Reference lists from the identified papers were manually searched. Systematic searches were performed from January 1, 1971, to October 1, 2025. Studies reporting on terminal ileum intubation and biopsy during colonoscopy were included. Case reports, letters, reviews, and animal studies were excluded. The primary outcomes were the diagnostic yield of terminal ileum intubation and the rate of necessitating a change in management. Data were extracted independently by three reviewers.

Thirty-six studies were included. The subtotal diagnostic yield and the rate of necessary change among the selected patients were much greater than those among the unselected patients (5.1% versus 2.5% and 1.5% versus 0.4%, respectively). In addition, the diagnostic yield was found more frequently for inflammatory bowel disease, anemia, abdominal pain, and chronic diarrhea than for the other indications (26.7%, 16.1%, 14.9%, 12.4%, and 3.2%, respectively). The yield of ileal histopathology with a normal endoscopic appearance was low in both unselected and selected patients (3.5% and 2.4%, respectively).

Terminal ileum intubation is recommended as gold standard for completing colonoscopy. Biopsy should be considered in patients with abnormal endoscopic findings or specific high-risk symptoms.

Regular exercise is fundamental for people with metabolic dysfunction-associated steatotic liver disease (MASLD), yet exercise maintenance is generally poor. This generative co-design process aimed to embed the voices and opinions of people with lived experience of MASLD and their care stakeholders to (i) frame barriers and enablers to exercise maintenance and (ii) highlight priorities for exercise-focused research agendas in MASLD.

A generative co-design framework was applied. Two virtual co-design sessions were undertaken: Session 1 – Framing the issue, where initial discovery was conducted with people with lived experience of MASLD; and Session 2 – Generative design and sharing ideas with lived experience partners and healthcare stakeholders. Sessions were audio-recorded and transcribed, and key determinants and considerations were discerned by two independent researchers.

Lived experience partners (n = 5, 53 ± 16 years, 40% male) ranked five equally important barriers to exercise maintenance: musculoskeletal and pain issues, lack of access to exercise equipment/facilities, cost, competing priorities, and low energy levels, which influenced core positive and negative determinants. Alongside lived experience partners, healthcare stakeholders (hepatologists [n = 3], exercise professionals [n = 3], 67% male) identified three core needs with eight considerations. Some disconnects in priorities were observed. Lived experience partners emphasized affordability, accessibility, and considerations for comorbidities, while healthcare partners advocated for research on natural history, prevention, behavior change, cost-effectiveness, and health system change.

This co-design methodology highlights unique consumer-informed research questions. Exercise interventions and their associated implementation trials will benefit from being co-designed with both people with MASLD and care stakeholders.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is now considered to be among the most prevalent chronic liver diseases worldwide. Its comprehensive management encompasses multiple stages, including risk assessment, early detection, stratified intervention, and long-term follow-up. Among these, improving diagnostic accuracy and optimizing individualized therapeutic strategies remain key challenges in both research and clinical practice. In recent years, artificial intelligence and smart devices have developed rapidly and have gradually been applied in the medical field, offering novel tools and pathways for MASLD risk stratification, non-invasive diagnosis, therapeutic evaluation, and patient self-management. This review summarizes the current applications of artificial intelligence and smart devices in MASLD care, highlights their benefits and limitations, and discusses future directions to support precision diagnosis and treatment strategies.

Gastric cancer remains a significant global health burden, with limited therapeutic options and poor clinical outcomes. Although conventional treatments such as surgery and chemotherapy are widely used, their effectiveness is often hindered by adverse effects and high recurrence rates, highlighting the urgent need for safer and more effective alternatives. Scleromitrion diffusum (Willd.) (S. diffusum), a well-established anticancer herb in traditional Chinese medicine, has demonstrated promising clinical potential against gastric cancer. This review systematically examines the bioactive components of S. diffusum and their multi-target mechanisms of action against gastric cancer. Key active compounds, including flavonoids, anthraquinones, and terpenoids, have been identified as exerting synergistic anti-gastric cancer effects. These compounds collectively target critical pathways in gastric cancer pathogenesis, including apoptosis induction, suppression of proliferation and angiogenesis, and immune modulation. The mechanistic elucidation presented in this review not only validates the traditional use of S. diffusum in cancer management but also provides a molecular basis for its potential application in precision medicine strategies for gastric cancer. Beyond summarizing existing evidence, this work highlights critical gaps in current knowledge and proposes essential directions for future research, providing important references for integrating traditional medicine with modern oncology approaches.

Khat (Catha edulis) is a plant native to East Africa and the Arabian Peninsula, chewed for its stimulant effects by millions worldwide. Its sympathomimetic properties, primarily due to cathinone and other pyrrolizidine alkaloids, resemble those of amphetamine. Emerging reports have linked khat use to the development of autoimmune hepatitis, supported by elevated autoimmune markers, characteristic liver biopsy findings, and clinical resolution following khat cessation or a prompt response to corticosteroid therapy without recurrence. In this review, we aimed to update knowledge on both acute and chronic forms of khat-associated AIH. We discuss cathinone metabolism, pharmacokinetics, and proposed mechanisms of khat hepatotoxicity. We also provide an updated synthesis of published cases of khat-associated autoimmune hepatitis, including our calculated Roussel-Uclaf Causality Assessment Method analysis and the simplified Hennes AIH score where data were available. Case presentations, diagnostic criteria, histopathological findings, and treatment approaches are summarized to help guide management.

Sterol regulatory element-binding protein 1 (SREBP1), a key regulator of lipogenesis, is highly expressed in tumors, but the mechanisms sustaining its elevated levels remain unclear. The role of UFMylation, a posttranslational modification, in modulating SREBP1 stability and tumor progression has not been explored. This study aimed to investigate the role of UFMylation in the progression of liver cancer.

Liquid chromatography-tandem mass spectrometry was employed to investigate the interacting proteins of ubiquitin-fold modifier 1-specific ligase 1 (UFL1). Knockdown of UFL1 and DDRGK domain-containing protein 1 (DDRGK1) was performed to assess SREBP1 stability. In vitro and in vivo models of hepatocellular carcinoma (HCC) were used to evaluate tumor progression. Clinical correlations between UFL1/DDRGK1 and SREBP1 levels were analyzed in HCC patient samples.

SREBP1 undergoes UFMylation, which synergizes with ubiquitination to reduce its stability. Depletion of UFL1 or DDRGK1 increased SREBP1 stability, driving HCC progression. Clinically, UFL1 and DDRGK1 levels were reduced in HCC tissues and inversely correlated with SREBP1 expression. Fatostatin (an SREBP1 inhibitor) enhanced the therapeutic effect of Lenvatinib in HCC models with low UFL1 expression.

UFMylation is a critical posttranslational modification that destabilizes SREBP1, and its dysregulation contributes to HCC progression. Targeting the UFMylation-SREBP1 axis, particularly through Fatostatin and Lenvatinib combination therapy, represents a novel therapeutic strategy for HCC.

Metabolic dysfunction-associated steatohepatitis (MASH) represents a critical step in the progression from simple fatty liver disease to more severe conditions such as cirrhosis and hepatocellular carcinoma, and it remains difficult to treat. Arctigenin (ATG), a monomer of Fructus Arctii, exhibits anti-inflammatory activity. Therefore, we aimed to examine its potential protective role against MASH and explore the underlying mechanisms.

Male C57BL/6 mice were divided into four groups: control, MASH, low-dose ATG (30 mg/kg/day), and high-dose ATG (120 mg/kg/day). MASH was induced through a choline-deficient, L-amino acid-defined high-fat diet for eight weeks, with concurrent preventive ATG administration. Liver injury, lipid metabolism, inflammation, oxidative stress, and fibrosis were assessed. Network pharmacology was employed to identify the potential protective mechanisms of ATG. Key factors were evaluated in vitro to verify the ATG targets.

ATG administration prevented the progression of MASH in a dose-dependent manner. High-dose ATG significantly reduced hepatic macrophage and neutrophil infiltration, serum enzyme levels, and lipid peroxidation, while enhancing antioxidant enzyme activity. Mechanistic network pharmacology identified modulation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome as the central pathway underlying ATG’s bioactivity. Functional analyses in lipopolysaccharide-stimulated RAW264.7 cells confirmed that ATG inhibited NLRP3 expression, pyroptosis-related protein cleavage (hereinafter referred to as GSDMD-N), and pro-inflammatory chemokine production in a concentration-dependent manner. Notably, ATG disrupted NLRP3/GSDMD-N axis activity in macrophages without causing cellular toxicity.

ATG may inhibit the inflammatory cascade primarily by targeting macrophage NLRP3 inflammasomes, thereby preventing the progression of MASH.

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.

Artemisia argyi H. Lév. & Vaniot essential oil (AAEO) holds significant pharmacological potential, but its application is constrained by hepatotoxicity. This study aimed to investigate the feasibility of reducing AAEO’s toxicity through storage and to evaluate changes in chemical composition, toxicity, and bioactivity.

Gas chromatography-mass spectrometry was used to analyze compositional changes during storage. Zebrafish acute toxicity tests and the liver-specific transgenic zebrafish model Tg(fabp10:EGFP) were used to assess toxicity. Antimicrobial, analgesic, and antioxidant assays evaluated variations in bioactivity.

Over the 150-day storage period, gas chromatography-mass spectrometry analysis identified 39 components. Zebrafish acute toxicity tests showed that the LD50 of AAEO stored for 0, 30, 60, 90, 120, and 150 days were 0.10 µL·mL−1, 0.10 µL·mL−1, 0.10 µL·mL−1, 0.11 µL·mL−1, 0.13 µL·mL−1, and 0.14 µL·mL−1, respectively, demonstrating a 40% reduction in acute toxicity after 150 days of storage. Using the liver-specific green fluorescent transgenic Tg(fabp10:EGFP) zebrafish model, the inhibition rates of AAEO on hepatic fluorescence intensity were measured at 68.5%, 43.5%, 42.6%, 37.8%, 34.6%, and 31.9% at different time points, confirming reduced hepatotoxicity after storage. Additionally, the antioxidant and analgesic activities of AAEO were significantly enhanced (p < 0.05) after storage, while the antibacterial activity decreased (p < 0.05).

After storage, AAEO significantly reduces hepatotoxicity, with a 40% decrease in acute toxicity after 150 days. Meanwhile, the antioxidant and analgesic activities of AAEO increase, while its antibacterial activity decreases after storage.