Pancreatic cystic neoplasms (PCNs) are increasingly detected in clinical practice, yet substantial variability exists in imaging interpretation and reporting, which may affect clinical decision-making. This guideline was developed to standardize diagnostic imaging evaluation and reporting for PCNs. A multidisciplinary expert panel conducted literature search and critical appraisal of domestic and international evidence, identified key clinical questions, and formulated recommendations using the Grading of Recommendations Assessment, Development and Evaluation framework. A modified Delphi consensus process and external review were performed to ensure the robustness of the recommendations. A total of 21 key questions were addressed, covering essential aspects of imaging evaluation and reporting for PCNs, including the preferred imaging modality for suspected lesions; standardized measurement of cyst size and mural nodules and their clinical significance; definitions of cyst wall and septal thickening; optimal imaging approaches for assessing the relationship between cystic lesions and the main pancreatic duct; measurement and evaluation of main pancreatic duct diameter and dilation; imaging-based classification of intraductal papillary mucinous neoplasms and serous cystic neoplasms; assessment of ductal obstruction, calcification, hemorrhage, and pancreatitis-related changes; criteria for suspicious lymph nodes; differentiation of PCNs from pancreatic pseudocysts or retention cysts; and recommended imaging modalities and follow-up intervals. This guideline provides a structured and evidence-based framework for imaging evaluation and reporting of PCNs, which may improve the consistency and clarity of imaging reports and support clinical decision-making.

The optimal management strategy for adults with immune-tolerant (IT) chronic hepatitis B infection remains undefined. This study aimed to investigate the efficacy and predictive factors of a pegylated interferon (Peg-IFN)-based treatment strategy in IT patients with chronic HBV infection.

In this pilot, open-label, prospective study, 286 patients aged 18 to 60 years with IT characteristics were enrolled and allocated to one of three groups. The combination group received Peg-IFN for 48–96 weeks, with tenofovir disoproxil fumarate (TDF) initiated at week 12 and continued through week 96 (n = 103). The monotherapy group received TDF monotherapy alone (n = 125), and the control group was monitored without therapeutic intervention (n = 58).

No patients in the control group met any predefined efficacy endpoints. Intention-to-treat analysis showed that patients in the combination group achieved significantly higher virological response rates (71.8% vs. 53.6%, p = 0.005), hepatitis B e antigen seroconversion rates (15.5% vs. 1.6%, p < 0.001), and hepatitis B surface antigen (HBsAg) loss rates (10.7% vs. 0%, p < 0.001) compared with those in the monotherapy group at week 96. In the combination group, the cumulative rate of HBsAg loss was 5.4% at week 48 and increased to 11.8% by week 96. Independent predictors of achieving either hepatitis B e antigen seroconversion or HBsAg loss were baseline age under 30 years (odds ratio = 0.217, 95% confidence interval: 0.048–0.976, p = 0.046) and a decline in HBsAg level greater than 1 log10 IU/mL by week 24 (odds ratio = 13.976, 95% confidence interval: 2.506–77.932, p = 0.003).

A Peg-IFN-based treatment strategy significantly increases response rates compared with TDF monotherapy or observation in patients with IT characteristics.

Antimitochondrial antibody (AMA)-negative primary biliary cholangitis (PBC) is a rare presentation of PBC that comprises 5%–10% of all PBC patients. The pathogenesis of AMA-negative PBC appears to be similar to that of AMA-positive PBC. AMA-negative PBC presents similarly to AMA-positive PBC, with symptoms of cholestasis, fatigue, and pruritus most commonly reported. Defective bicarbonate production, resulting in acidification of bile and bile acids, has been proposed as the primary mechanism of damage to bile ducts and hepatocytes and is reflected in elevations of alkaline phosphatase and aminotransferases. Chronic damage can lead to the development of cirrhosis. The diagnosis is made by the finding of AMA negativity by ELISA or assays of similar sensitivity and a positive PBC-specific antinuclear antibody (ANA; anti-glycoprotein 210 and anti-speckled 100 kDa protein) test. In cases in which anti-glycoprotein 210 and anti-speckled 100 kDa protein assays are also negative, a liver biopsy is required to make the diagnosis after exclusion of other causes of cholestasis by magnetic resonance cholangiopancreatography or endoscopic retrograde cholangiopancreatography. Treatment for AMA-negative PBC is the same as for AMA-positive cases, with ursodeoxycholic acid as the first-line treatment. Current treatment is most effective in early stages, where it slows but does not eliminate progression. Risk stratification by validated tools such as the GLOBE and UK-PBC scores remains useful in AMA-negative PBC.

Unlike the traditional staging treatment of tumors, the core of “Green Tumor Treatment” is to divide the treatment of tumors into three stages: Hegemony (directly targeting the cancer focus), Kingship (supporting the body’s vital energy and eliminating pathogenic factors), and Imperialism (improving the internal environment), based on the urgency of the tumor and the patient’s physical condition. This approach guides the clinical treatment of tumors. Its treatment system incorporates all minimally invasive and low-damage treatment methods, combining internal and external treatments, traditional Chinese medicine and Western medicine, as well as local and systemic treatments. It aims to maximize treatment outcomes while ensuring the patient’s quality of life, which is highly consistent with the treatment goals for primary liver cancer. This review aims to explore the integrated Traditional Chinese and Western medicine treatment model for primary liver cancer under the guidance of the Green Tumor Treatment concept.

Metabolic dysfunction–associated steatotic liver disease (MASLD), defined by the American Association for the Study of Liver Diseases as hepatic steatosis with at least one cardiometabolic risk factor, affects approximately 30–40% of adults worldwide. This condition may progress to fibrosis, cirrhosis, and hepatocellular carcinoma. The rising prevalence, alongside obesity and type 2 diabetes, underscores the need for early risk stratification and integrated therapeutic strategies. Circadian homeostasis, orchestrated by the suprachiasmatic nucleus and core clock gene feedback loops, synchronizes hepatic metabolic pathways with environmental light–dark cycles. The objective of this review is to evaluate the role of circadian disruption and metabolic dysfunction in the development of hepatic steatosis, as well as to assess current and potential treatment modalities for both disorders. Circadian disruption through shift work, artificial light at night, sleep restriction, and chrono-nutritional misalignment destabilizes hepatic clocks, promoting insulin resistance, dyslipidemia, inflammation, and steatosis. Experimental models demonstrate that clock gene dysfunction alone can induce steatohepatitis, while progressive MASLD further impairs central circadian regulation, establishing a self-reinforcing chrono-metabolic cycle. Pharmacologic therapies, including glucagon-like peptide-1 receptor agonists and thyroid hormone receptor-β agonists, improve histologic endpoints and fibrosis regression, although heterogeneity among clinical trials precludes direct comparison. Recent evidence characterizing MASLD as a predominantly nocturnal metabolic disorder further highlights persistent nighttime insulin dysregulation despite weight loss, emphasizing the potential role of circadian-targeted interventions such as melatonin. In conclusion, the peripheral circadian clock is intricately linked with MASLD pathogenesis, and metabolic dysfunction, in turn, disrupts circadian pathways. Several pharmacologic therapies offer potential for the treatment of MASLD and circadian dysfunction.

Liver fibrosis is a pivotal and reversible stage in the progression of chronic liver disease. However, the mechanisms underlying fibrosis reversal remain unclear, and effective diagnostic biomarkers are lacking in clinical practice. In this study, we aimed to elucidate the role and molecular mechanisms of glutathione S-transferase Mu 3 (GSTM3) in liver fibrosis reversal, and preliminarily determine whether GSTM3 can serve as a novel biomarker for liver fibrosis reversal.

Carbon tetrachloride-induced mouse models of liver fibrosis and spontaneous reversal were established. Proteomic analysis was used to identify proteins shared between liver tissue and serum that were continuously downregulated during fibrosis reversal. The expression of GSTM3 was evaluated in the livers of mice undergoing fibrosis reversal and in clinical samples from patients with liver fibrosis. Hepatic stellate cells (HSCs) were transfected with Gstm3-silencing RNA or an overexpression plasmid to assess the effects on fibrosis markers. RNA sequencing analyses were performed, and the underlying molecular mechanisms were investigated.

Proteomic analysis revealed significantly decreased GSTM3 levels in both hepatic tissue and serum in mice undergoing fibrosis reversal, and its expression was negatively correlated with the extent of reversal. GSTM3 levels were markedly increased in the hepatic tissue and serum of patients with liver fibrosis. GSTM3 expression was upregulated in transforming growth factor-β-stimulated HSCs. GSTM3 knockdown inhibited the expression of fibrosis markers, such as collagen type I α1 and tissue inhibitor of metalloproteinase 1, whereas its overexpression promoted their expression. Mechanistic studies indicated that GSTM3 knockdown activated peroxisome proliferator-activated receptor γ (PPARγ) signaling and downregulated its downstream targets, cluster of differentiation 36 and fatty acid-binding protein 4, thereby suppressing HSC activation.

GSTM3 knockdown promotes liver fibrosis reversal via PPARγ signaling-mediated inhibition of HSC activation. Therefore, GSTM3 is a promising therapeutic target and diagnostic biomarker for liver fibrosis.

Metabolic dysfunction-associated fatty liver disease (MAFLD) represents a predominant cause of chronic liver disease, underscoring the demand for accessible, non-invasive diagnostic tools. Tongue diagnosis in Traditional Chinese Medicine provides a distinctive perspective on systemic health, though it remains largely subjective. This study aimed to develop an interpretable multimodal deep learning model for MAFLD screening by integrating quantitative tongue image features with routine clinical data.

From 904 screened candidates, 477 subjects (157 healthy, 320 MAFLD) were included and randomly allocated to training, validation, and test sets in an 8:1:1 ratio. All participants underwent standardized tongue imaging (International Commission on Illumination L*a*b color features) and comprehensive clinical evaluation. We constructed a dual-stream deep learning model, combining a ConvNeXt-Tiny network for tongue images and a multilayer perceptron for clinical variables. Feature fusion was achieved via a Dynamic Affine Feature Transformation module, and the model was trained using weighted cross-entropy loss.

MAFLD patients showed significant metabolic abnormalities compared to healthy controls. A progressive decrease in tongue yellowness (b* value) was observed with advancing fibrosis. On an independent test set (n = 48), the multimodal model achieved 97.92% accuracy, Quadratic Weighted Kappa of 0.9538, and 96.88% sensitivity, and 100% specificity, outperforming single-modality and serological models. Interpretability analyses confirmed the model’s focus on clinically relevant tongue regions and key metabolic drivers.

We developed an accurate and interpretable multimodal model that synergizes tongue image features with metabolic indicators for MAFLD screening. This approach presents a promising, low-cost tool potentially well-suited for resource-limited settings.

Alpinia calcarata (A. calcarata) Roscoe (Family: Zingiberaceae) is a rhizomatous perennial herb used in traditional medicine to treat inflammatory conditions. This study aimed to develop a topical emulgel dosage form by incorporating the essential oil of A. calcarata rhizome and to investigate it’s in vitro anti-inflammatory activity. A thin-layer chromatographic fingerprint of the essential oil of A. calcarata rhizome was developed. Then, an emulsion base containing plant oil was formulated and incorporated within a Carbopol gel base. The physical characteristics of this formulation were evaluated subsequently. The anti-inflammatory mechanism of the emulgel was determined by in vitro blood cell membrane stabilization assay and thrombolytic activity assay. The results were statistically analyzed by one-way analysis of variance. The thin-layer chromatographic fingerprint of the test oil demonstrated several bands with unique retention factor values. The formulated herbal emulgel was white, viscous, and homogeneous in appearance. The spreadability was 118 g·cm/M, and the pH of the emulgel was 6.30 at 25°C. The A. calcarata emulgel significantly (p < 0.05) inhibited heat-induced in vitro hemolysis, with the highest activity at a 50 µg/mL dose (87.68 ± 0.35%) compared to the placebo. Furthermore, this activity was found to be dependent on the essential oil concentration (r2 = 0.99) of the emulgel. Therefore, it was concluded that the essential oil of A. calcarata rhizome is an effective active ingredient to be used in a topical emulgel formulation, whereas the diverse phytochemicals present in the essential oil would be the underlying source of its anti-inflammatory activity.

The long-term clinical outcomes of patients with hepatitis B virus (HBV)-related cirrhosis receiving nucleos(t)ide analog (NA) therapy according to virological response patterns remain inadequately defined. This study aimed to investigate the association between virological response patterns and clinical outcomes in a large, long-term, real-world cohort.

This retrospective–prospective cohort study enrolled patients with HBV-related cirrhosis receiving NA therapy from 2009 to 2019. According to the serum HBV DNA levels during the initial two years of antiviral treatment, patients were categorized as having a complete (CVR) or partial virological response (PVR). Patients with CVR were further stratified according to their dynamic HBV DNA changes during follow-up into maintained virological response (MVR) or virological breakthrough (VBT) patterns. The primary clinical outcomes included hepatocellular carcinoma (HCC), acute-on-chronic liver failure, and liver-related death. Secondary endpoints included recompensation and progression to decompensation. Cox proportional hazards regression was used to assess the association between virological response patterns and clinical endpoints.

In total, 1,869 patients were enrolled. During a median follow-up of seven years, the MVR, VBT, and PVR rates were 65.4%, 26.5%, and 8.1%, respectively. The cumulative serum hepatitis B surface antigen (HBsAg) clearance rate was 9.8%. Moreover, 34.9% of patients with HBsAg < 100 IU/mL at baseline experienced HBsAg clearance. Compared with patients with VBT and PVR, those with MVR had a lower five- and ten-year cumulative incidence of HCC in both the compensated (five-year: 10.1% vs. 17.0%; ten-year: 14.2% vs. 33.6%; P < 0.001) and decompensated cirrhosis subgroups (five-year: 19.5% vs. 36.7%; ten-year: 25.7% vs. 49.7%; P < 0.001). Similarly, patients with MVR also had a lower cumulative incidence of liver-related death. Additionally, a higher hepatic recompensation rate was observed in patients with MVR than in those with VBT (34.1% vs. 22.5%, P < 0.001). Importantly, patients achieving HBsAg clearance and undetectable serum HBV DNA levels (“functional cure” during ongoing NA therapy) had the lowest five- and ten-year cumulative incidence of HCC (3.9% and 8.7%, respectively).

Patients with long-term MVR exhibited a lower incidence of HCC and liver-related death in both compensated and decompensated HBV-related cirrhosis subgroups, especially those achieving “functional cure.” However, more than 30% of patients experienced PVR or VBT during long-term NA antiviral therapy. These findings highlight the importance of long-term, rigorous monitoring after initial CVR to optimize outcomes and support clinical decision-making.

Chronic pancreatitis is an inflammatory disease and is difficult to manage despite advancements in medical science. This study examined the effect of water/ethanol extracts of Justicia carnea leaves on oxidative stress and glucagon expression in a mouse model of chronic pancreatitis induced by trinitrobenzenesulfonic acid (TNBS).

Twenty-five male Swiss albino mice were randomized and treated intrarectally with vehicle (the control group) or TNBS. Some TNBS-treated mice were treated orally with 200 mg/kg or 400 mg/kg J. carnea extracts, or with the positive control, 500 mg/kg sulfasalazine, every other day on three occasions. Oxidative stress markers and pancreatic glucagon expression were assessed.

Compared with the healthy control mice, treatment with TNBS significantly decreased the levels of pancreatic glutathione (0.89 µmol/g tissue vs. 7.16 µmol/g tissue in the control) and glutathione peroxidase activity, but significantly increased the levels of α-amylase and lipase activities, lipid peroxidation, total antioxidant capacity, and nitric oxide, as well as serum C-reactive protein (P < 0.05 for all), accompanied by severe inflammation and reduced glucagon expression in the pancreatic tissues. The toxic effects of TNBS were significantly mitigated by treatment with J. carnea extracts.

These findings provide evidence that treatment with J. carnea extracts inhibited oxidative stress and preserved glucagon expression in the pancreatic tissues of mice.