Metabolic-associated steatohepatitis (MASH) is an advanced and progressive liver disease that potentially causes cirrhosis and hepatocellular carcinoma. Exercise is a crucial and effective intervention for ameliorating metabolic dysfunction-associated steatotic liver disease. This study aimed to provide a comprehensive understanding of the underlying mechanisms of MASH, which benefit a broad spectrum of MASH patients, including those who have difficulty engaging in physical activity.

We established a mouse model of MASH and selectively knocked down L-type amino acid transporter 1 and alanine-serine-cysteine transporter 2. Mice were fed a high-fat high-cholesterol diet and subjected to either short- or long-term exercise regimens. We assessed the phosphorylation and activity of branched-chain alpha-keto acid dehydrogenase (BCKDH) as well as branched-chain amino acid (BCAA) content in skeletal muscle following exercise.

Short-term exercise significantly reduced hepatic steatosis and inflammation without causing notable changes in body weight. It also enhanced BCKDH activity in skeletal muscle and decreased hepatic BCAA accumulation. Muscle-specific overexpression of BCKDH further promoted BCAA catabolism and significantly attenuated hepatic steatosis and inflammation in high-fat high-cholesterol-fed mice. In contrast, muscle-specific L-type amino acid transporter 1 knockdown, which suppresses BCAA uptake, markedly abolished these beneficial effects. Interestingly, BCKDH overexpression in muscle increased glutamine levels in both the blood and liver. Hepatic alanine-serine-cysteine transporter 2 knockdown, which inhibited glutamine uptake, lessened the protective effect of exercise on MASH. Further in vitro study revealed that glutamine derived from myocytes improved redox homeostasis and inhibited lipid accumulation in hepatocytes.

Short-term exercise enhances BCAA catabolism in skeletal muscle and promotes glutamine production, which circulates to the liver to improve redox balance and alleviate MASH.

Extrahepatic portosystemic shunts (EPS) are abnormal connections between the portal and systemic circulations. Acquired EPS occur most commonly in adults and are usually associated with portal hypertension due to cirrhosis. Acquired EPS cases can be further subdivided into two types: variceal (pre-existing) EPS and non-variceal EPS (NVEPS). Variceal EPS arise from originally small vessels with pre-existing dual portal and systemic drainage. Due to elevated portal pressure, these vessels dilate and undergo a reversal of flow, sending blood back to the systemic circulation. A much less common and, therefore, underappreciated subset of acquired EPS is NVEPS, which consists of aberrant connections that did not previously exist between the portal vein and large systemic vessels, usually in the presence of portal hypertension. Neoangiogenesis results in the development of abnormal anastomoses between the portal vein and other large veins, resulting in splenorenal, gastrorenal, portocaval, and mesocaval shunts. While not uncommon, they are frequently overlooked in the diagnosis and treatment of portal hypertension and can pose significant diagnostic and therapeutic challenges. Because the treatment of variceal EPS and NVEPS can differ markedly, it is important to correctly diagnose NVEPS and institute appropriate management. The aim of this article was to review acquired EPS, with particular attention to NVEPS, updating the pathogenesis, diagnosis, and treatment.

The causal biomarkers for metabolic dysfunction-associated steatotic liver disease (MASLD) and their clinical value remain unclear. In this study, we aimed to identify biomarkers for MASLD and evaluate their diagnostic and prognostic significance.

We conducted a Mendelian randomization analysis to assess the causal effects of 2,925 molecular biomarkers (from proteomics data) and 35 clinical biomarkers on MASLD. Mediation analysis was performed to determine whether clinical biomarkers mediated the effects of molecular biomarkers. The association between key clinical biomarkers and MASLD was externally validated in a hospital-based cohort (n = 415). A machine learning–based diagnostic model for MASLD was developed and validated using the identified molecular biomarkers. Prognostic significance was evaluated for both molecular and clinical biomarkers.

Six molecular biomarkers—including canopy FGF signaling regulator 4 (CNPY4), ectonucleoside triphosphate diphosphohydrolase 6 (ENTPD6), and major histocompatibility complex, class I, A (HLA-A)—and eight clinical biomarkers (e.g., serum total protein (STP)) were identified as causally related to MASLD. STP partially mediated the effect of HLA-A on MASLD (23.61%) and was associated with MASLD in the external cohort (odds ratio = 1.080, 95% confidence interval: 1.011–1.155). A random forest model demonstrated high diagnostic performance (AUC = 0.941 in training; 0.875 in validation). High expression levels of CNPY4 and ENTPD6 were associated with the development of and poorer survival from hepatocellular carcinoma. Low STP (<60 g/L) predicted all-cause mortality (HR = 2.50, 95% confidence interval: 1.22–5.09).

This study identifies six causal molecular biomarkers (e.g., CNPY4, ENTPD6, HLA-A) and eight clinical biomarkers for MASLD. Notably, STP mediates the effect of HLA-A on MASLD and is associated with all-cause mortality.

Patients with chronic hepatitis B virus (HBV) infection in the immune-tolerant phase may still experience hepatic inflammation and disease progression, and could benefit from early antiviral treatment. This study aimed to investigate changes in the cumulative hepatitis B surface antigen (HBsAg)/HBV DNA ratio in immune-tolerant patients during the transition to the immune-active phase, and to evaluate its potential in predicting the risk of disease progression.

This longitudinal study included 127 untreated immune-tolerant patients, who were followed for up to 10 years. An independent cohort of 109 subjects was retrospectively enrolled for external validation. The relationship between the cumulative HBsAg/HBV DNA ratio and the duration of immune tolerance or transition to the immune-active phase was examined. The predictive value of the ratio was assessed and validated.

The relationship between the cumulative HBsAg/HBV DNA ratio and disease progression risk showed a non-linear pattern: below a ratio of 1.791, the risk of disease progression decreased rapidly as the ratio increased; above 1.791, the risk plateaued. The area under the curve for predicting disease progression was 0.67, 0.64, and 0.85 for cumulative HBsAg, HBV DNA, and the HBsAg/HBV DNA ratio, respectively. Multivariable Cox regression analysis revealed the cumulative HBsAg/HBV DNA ratio as an independent predictor of disease progression, with higher ratios associated with a lower risk. Prediction models incorporating this ratio were developed and externally validated, demonstrating strong performance and clinical utility.

The cumulative HBsAg/HBV DNA ratio is an independent factor influencing the duration of immune tolerance and shows superior predictive performance. It may serve as a valuable marker for assessing the risk of disease progression in patients with chronic HBV infection.

Artificial intelligence (AI) is profoundly transforming the paradigm of solid tumor drug development. By integrating multi-omics data, spatial transcriptomics, and advanced computational models, AI has significantly accelerated the discovery and validation of new targets, compressing the traditional ten-year research and development cycle to two to three years. Generative AI platforms have optimized small molecule inhibitors, biologics, and messenger RNA vaccines, achieving breakthroughs in overcoming tumor heterogeneity, improving efficacy, and predicting drug resistance. However, clinical translation still faces challenges such as data bias, algorithm transparency, and the validation gap between models and real-world human experience. This review aims to systematically elaborate on the transformative role of AI in solid tumor drug development and to promote interdisciplinary cooperation as well as the construction of ethical frameworks to enable the full realization of precision oncology.

Colorectal cancer (CRC) is a type of cancer that originates in the colon or rectum from precancerous polyps, which can evolve into cancerous growths over time. This review aimed to provide a comprehensive analysis of CRC, its subtypes, clinical manifestations, point-of-care diagnostic approaches, and management strategies. The clinical presentation of CRC often includes symptoms such as blood in stool, changes in bowel habits, abdominal discomfort, weight loss, fatigue, a feeling of incomplete bowel emptying, and anemia. The identification of these signs prompts healthcare professionals to initiate diagnostic measures without delay. Point-of-care diagnosis plays a pivotal role in the early detection of CRC, employing screening tests such as stool tests and colonoscopies. These diagnostic modalities enable healthcare professionals to identify precancerous polyps or early-stage tumors, facilitating timely intervention and significantly improving treatment outcomes. Adherence to screening guidelines is crucial for the prevention and early detection of CRC. Despite advancements in screening and treatment options, there remains a crucial need for more specific, minimally invasive screening methods with minimal side effects. By improving current detection methods, a better screening approach for CRC can be developed. Recent advancements, including single-cell sequencing, spatial transcriptomics, and artificial intelligence integration, hold great promise for enhancing early diagnosis and advancing personalized treatment strategies. Moreover, a healthy lifestyle, including a balanced diet, regular exercise, no tobacco use, and limited alcohol consumption, can significantly lower the risk of CRC. By emphasizing the importance of lifestyle modifications, early screening, and timely intervention, healthcare professionals can significantly reduce the burden of CRC and improve patient outcomes.

Proper nutritional management has been shown to reduce complications and lead to better clinical outcomes. However, inaccurate nutritional screening and assessment, inappropriate nutrition support, and deviations from suggested guidelines were observed in clinical practice. We aimed to investigate the nutritional status and support of hospitalized patients with neurological diseases to identify deficiencies in nutritional assessment and treatment.

A self-designed questionnaire, developed through a literature review, group discussions, and expert consultation, was converted into an electronic form to conduct a cross-sectional survey in a tertiary-level general hospital. The patients’ basic information and the first nutrition assessment were filled out upon admission. The final nutrition assessment were logged at discharge, transfer out, or death. Two-person cross-entry was used to ensure the accuracy of data input.

A total of 620 patients were enrolled in this study. Of these, 24.4% were at nutritional risk upon admission, and 22.7% were identified as at nutritional risk in the final assessment. There were no statistically significant differences in nutritional status between the first and final assessments, except for serum albumin concentration. A total of 118 patients (19.0%) received nutrition therapy. Complications occurred in 35 (45.5%) patients treated with enteral nutrition and 29 (30.5%) patients treated with parenteral nutrition.

The incidence of nutritional risk in inpatients with neurological diseases enrolled in this study was relatively low. However, nutritional treatment in this study was not sufficiently standardized. Nurses are needed to receive relevant professional training to improve quality of nutritional interventions.

Mucinous cystic neoplasms (MCNs) are rare pancreatic lesions that often go undiagnosed due to their asymptomatic nature. Though typically benign, they can harbor malignant potential, making early detection and treatment essential. This case report presents a 32-year-old female with intermittent epigastric pain, who was found to have a cystic lesion in the pancreatic tail, diagnosed as an MCN through endoscopic ultrasound and fine-needle aspiration. The patient underwent a spleen-sparing distal pancreatectomy, which was complicated by a peri-pancreatic abscess that required drainage. This case highlights the importance of distinguishing MCNs from other pancreatic cystic lesions, as misdiagnosis or delayed intervention can lead to adverse outcomes. It underscores the need for vigilant diagnostic imaging and individualized treatment strategies, particularly in young patients, to avoid unnecessary morbidity and ensure optimal outcomes. The report contributes to the growing understanding of MCNs, emphasizing early diagnosis, tailored surgical management, and the significance of postoperative care.

Soft tissue cytopathology plays a vital role in the diagnosis and management of soft tissue neoplasms, necessitating a standardized classification system to improve diagnostic accuracy and guide clinical decision-making. This article provides a concise review of the World Health Organization (WHO) Reporting System for Soft Tissue Cytopathology and presents a practical diagnostic approach to soft tissue cytopathology.

The WHO Reporting System is reviewed in conjunction with relevant literature. The reporting system employs a six-category framework: non-diagnostic, benign, atypical, soft tissue neoplasm of uncertain malignant potential, suspicious for malignancy, and malignant. Each category is associated with a corresponding risk of malignancy and recommended clinical management guidelines. This classification aligns with the WHO Classification of Soft Tissue and Bone Tumours (5th edition) and incorporates cytomorphologic features, ancillary studies, and clinical correlation to enhance diagnostic reproducibility and communication among pathologists and clinicians.

The system supports a probabilistic approach to risk stratification, enabling more consistent diagnostic and therapeutic strategies.

As molecular diagnostics and immunocytochemistry continue to advance, this framework provides a robust foundation for the interpretation of soft tissue fine-needle aspiration biopsies and optimized patient care.

Inherited metabolic liver diseases (IMLDs) have complex etiologies and vary widely in clinical presentation, with a significant overall incidence. With the advancements in diagnostic and treatment technologies, an increasing number of children with inherited metabolic diseases are surviving into adolescence and adulthood. These advancements have improved our understanding of the IMLD disease spectrum and clinical outcomes. This study aimed to analyze changes in the disease spectrum and epidemiological characteristics of inherited metabolic liver diseases (IMLD) over the past 20 years in two specialized liver disease hospitals in northern China.

A retrospective analysis was conducted on IMLD cases diagnosed between January 1, 2002, and December 31, 2023, at two liver disease specialty hospitals in Beijing. Data were obtained from inpatient and outpatient hospital information systems, with diagnoses based on national and international IMLD diagnosis and treatment guidelines.

A total of 2,103 IMLD patients were analyzed, including 1,213 adults and 890 children. IMLD accounted for 4.58‰ of hospitalized liver disease patients during this period. The most common IMLD was Wilson’s disease, comprising 68% of all IMLD cases. The number of diagnosed IMLD types increased from 15 to 32 across two 11-year periods (2002–2012 and 2013–2023). Among pediatric patients, glycogen storage disease and Alagille syndrome were more prevalent in those under one year of age, while Wilson’s disease was prevalent across all age groups. In adult IMLD patients, Wilson’s disease, polycystic liver disease, and hereditary hyperbilirubinemia were more frequently observed.

Over the past 20 years, both the number of diagnosed IMLD cases and disease diversity have significantly increased, with Wilson’s disease remaining the most prevalent IMLD. These findings provide valuable insights for the long-term management of IMLD patients and the allocation of healthcare resources.