Pancreatic cancer remains a highly lethal malignancy owing to the difficulty of early detection. In 2021, the Chinese Consensus on Early Screening and Surveillance for Pancreatic Cancer in High-risk Individuals was first established. However, the evidence landscape has evolved rapidly, necessitating an updated, evidence-based framework tailored to the Chinese healthcare context. This revised consensus aims to standardize the early screening and surveillance process for high-risk populations in China. A multidisciplinary expert panel comprising 53 specialists from 17 provincial-level regions systematically reviewed the literature using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) methodology. A modified Delphi process was employed, with consensus predefined as ≥75% agreement. The panel formulated 26 evidence-based recommendations covering screening objectives, the definition of high-risk populations (hereditary susceptibility, new-onset diabetes, chronic pancreatitis, and pancreatic cystic neoplasms), age at screening initiation, surveillance intervals, imaging modalities (magnetic resonance imaging/magnetic resonance cholangiopancreatography, endoscopic ultrasound, computed tomography), surgical indications, and lifestyle modifications. Of these recommendations, 14 are strong and 12 are weak, supported by evidence levels ranging from A to D. Implementation of this consensus in clinical practice will help improve the early diagnosis of stage I pancreatic cancer and high-grade precursor lesions, thereby advancing standardized multidisciplinary care and ultimately improving patient outcomes in China.

The optimal surgical management for spontaneous supratentorial intracerebral hemorrhage (SSICH) remains controversial because conventional approaches often fail to balance rapid decompression with effective hematoma evacuation. This study aimed to evaluate the efficacy and safety of new combined surgical strategies (“two-in-one” and “three-in-one”) versus conventional methods for SSICH.

This retrospective cohort study included 451 SSICH patients treated between January 2019 and December 2023. Based on clinical severity, patients were stratified into Group I (non-herniation, n = 374) and Group II (herniation, n = 77). Within each subgroup, patients were further categorized by treatment period: a historical control cohort (2019–2020) receiving conventional surgery, and an intervention cohort (2021–2023) receiving combined strategies (“two-in-one” for Group I; “three-in-one” for Group II). Outcomes included decompression time, hematoma evacuation rate, complications, and six-month functional recovery (Glasgow Outcome Scale/modified Rankin Scale), were compared.

In Group I, the “two-in-one” strategy achieved faster decompression (4.65 min) and a high evacuation rate (92.15%), which was comparable to neuroendoscopy alone (90.58%) and significantly higher than stereotactic aspiration alone (44.55%). This was associated with improved six-month outcomes (poor outcome rates were 39.39%, 54.35%, and 42.86% in Groups I-A, I-B, and I-C, respectively, overall P = 0.034). In Group II, the “three-in-one” strategy demonstrated shorter decompression time (4.73 vs. 37.85 min, P < 0.001) and higher evacuation rates (80.51% vs. 63.50%, P < 0.001) than decompressive craniectomy alone. Logistic regression further supported the prognostic advantage of the “two-in-one” strategy in Group I.

These combined strategies may integrate the advantages of multiple techniques to enable rapid decompression and effective hematoma clearance in SSICH. Prospective studies are warranted.

Steatotic donor livers are highly susceptible to post-transplant dysfunction; however, the underlying mechanisms remain incompletely understood. This study aimed to investigate the role of galectin-3 (LGALS3)-mediated pyroptosis in steatotic liver graft injury and explore its therapeutic potential.

A mouse model of steatotic liver transplantation was established. Graft tissues were subjected to RNA sequencing to identify key regulators. In vitro, LGALS3 was modulated in steatotic hepatocytes under ischemia/reperfusion stress to assess its impact on the NLRP3 inflammasome and pyroptosis. The regulatory mechanism by which LGALS3 modulates NLRP3 ubiquitination was further examined. Finally, the therapeutic efficacy of LGALS3 inhibition was evaluated in an orthotopic liver transplantation model.

Transcriptomic analysis identified LGALS3 as a key upregulated molecule in steatotic grafts, associated with pyroptosis pathways. In vitro, LGALS3 overexpression enhanced NLRP3 inflammasome activation and pyroptotic cell death, whereas LGALS3 knockdown exerted protective effects. Mechanistically, LGALS3 modulated NLRP3 inflammasome activity by regulating its ubiquitination. In vivo, pharmacological inhibition of LGALS3 significantly improved graft function, reduced histological injury, suppressed pyroptosis, and prolonged recipient survival.

This study demonstrates that LGALS3 drives steatotic graft injury by promoting NLRP3-mediated pyroptosis through the regulation of ubiquitination. These findings identify LGALS3 as a promising therapeutic target for improving the outcomes of liver transplantation using steatotic donor organs.

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 intestinal barrier, a critical interface between the body and the external environment, is essential for maintaining internal homeostasis. Comprising mechanical, chemical, immune, and biological components, its dysfunction underpins multiple gastrointestinal pathologies. Circular RNAs (circRNAs), covalently closed non-coding RNAs, have emerged as central regulators of gut barrier homeostasis. This review synthesizes advances in circRNA roles in intestinal stem cell renewal, apoptosis-proliferation balance, microbiome interactions, and immune regulation. Key findings highlight circRNA networks operating via competitive endogenous RNA mechanisms, protein interactions, and translational potential to influence barrier function. We further discuss circRNAs as diagnostic biomarkers in inflammatory bowel disease and their therapeutic potential in barrier-related pathologies. Advances in RNA nanotechnology (e.g., lipid nanoparticles) and synthetic biology position engineered circRNAs as next-generation therapies for precision intervention in gastrointestinal disorders. Importantly, this review also critically examines the current limitations of these translational approaches, including delivery challenges, safety considerations, and the preliminary nature of many preclinical findings, providing a balanced perspective on the path from bench to bedside.

Primary sclerosing cholangitis (PSC) is an immune-mediated cholestatic liver disease. Its molecular etiology remains poorly defined, hindering the development of mechanism-based diagnostics and therapies. Therefore, this study aimed to identify key molecular drivers and causal biomarkers of PSC by integrating transcriptomics, machine learning, and genetic causal inference.

We deployed an integrated computational framework combining transcriptomics, network biology, machine learning, and genetic causal inference. Peripheral blood transcriptomes from PSC patients and controls were analyzed to identify disease-associated modules. Candidate genes were refined via protein-protein interaction networks and a multi-algorithm machine learning screen. Causal inference was performed using two-sample Mendelian randomization, integrating plasma protein quantitative trait loci with PSC genome-wide association study summary statistics.

Transcriptomic analysis revealed a PSC-associated module enriched in ribosome biogenesis and protein homeostasis pathways. A machine learning-optimized nine-gene signature (including PTMA, SUMO1, Shwachman-Bodian-Diamond syndrome (SBDS), RPL7, EIF1AX, ANP32A, PCNA, FAM98A, and MPHOSPH6) achieved high diagnostic accuracy (mean AUC = 0.908) and was consistently downregulated in PSC. This signature was linked to a remodeled immune microenvironment characterized by myeloid skewing and specific transcriptional-immune covariation patterns. Mendelian randomization identified SBDS as a putatively causal protective factor, where genetically instrumented higher plasma SBDS protein levels were robustly associated with a lower PSC risk (IVW OR = 0.525, 95% CI: 0.356–0.773, P = 0.001). Sensitivity analyses supported the validity of the Mendelian randomization assumptions.

Our study establishes disrupted ribosome homeostasis as a causal pathway in PSC and nominates plasma SBDS as a high-confidence diagnostic biomarker and therapeutic target. The integrative framework provides a generalizable strategy for discovering causal biomarkers in complex diseases.

Primary liver cancer is one of the most common malignant tumors in China, which seriously threatens people’s lives and health. In recent years, with the advancement of basic and clinical research, the diagnosis and treatment methods for primary liver cancer have been continually enriched. Traditional Chinese medicine (TCM) has played an important role in the diagnosis and treatment of primary liver cancer, but there is no unified standard for differentiation and treatment, and efficacy evaluation. In order to further standardize the TCM diagnosis and treatment of primary liver cancer, according to the requirements of TCM standardization and related technical guidance documents, the drafting team compiled this guideline through literature research, expert interviews, questionnaire surveys, consensus meetings, etc., for reference by clinicians. This guideline is approved and issued by the China Association of Chinese Medicine, standard number: T/CACM 1575-2024.

Pancreatic solid tumors encompass diverse pathological subtypes. Objective, accurate, and comprehensive imaging examinations and diagnostic reports are essential for preoperative staging, treatment planning, and prognostic evaluation. Currently, China lacks corresponding guidelines or consensus documents, leading to prominent issues including subjective diagnostic reports, incomplete descriptions, and inconsistent terminology. The present guideline was developed to standardize diagnostic imaging reporting of pancreatic solid tumors in China. Relevant domestic and international evidence on imaging examination techniques, key reporting elements, and diagnostic criteria was systematically reviewed and synthesized. This guideline was developed by a multidisciplinary expert panel through systematic evidence retrieval and appraisal, GRADE-based recommendation grading, modified Delphi consensus, and external review. A total of 20 evidence-based recommendations, 13 strong and 7 weak, were formulated, in aspects of imaging examination and diagnostic reporting standards, including the measurement of the tumor size of pancreatic solid tumors, assessment of the obstruction of the main pancreatic duct and common bile duct, definition, assessment, and clinical significance of pancreatic parenchymal atrophy, the assessment of obstructive acute pancreatitis, pseudocysts/retention cysts, and peripancreatic vessels, criteria for resectability, regional lymph node assessment, criteria for suspicious lymph nodes and descriptions of their specific location, and detection of hepatic and peritoneal metastases. Implementation of this guideline in clinical practice will help standardize the accuracy and consistency of diagnostic imaging reports for pancreatic solid tumors in China, thereby advancing standardized imaging diagnosis and informing clinical treatment decisions.

Nonalcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder with a complex pathogenesis. Although epitranscriptomic modifications such as N6-methyladenosine (m6A) have been implicated in NAFLD, the role of N1-methyladenosine (m1A) and its regulators is largely unexplored. Recently, YTHDF1, a well-characterized m6A reader, was also shown to recognize m1A; however, the functional consequences of this dual specificity are unknown. This study aimed to investigate the role of YTHDF1 in NAFLD pathogenesis and to explore whether its function is mediated through recognition of RNA methylation modification on specific target mRNAs.

Expression of YTHDF1 in NAFLD was analyzed in the GEO database. Loss-of-function studies for YTHDF1 were conducted in vivo (high-fat diet-fed mice) and in vitro (free fatty acid-treated HepG2 cells) in models of NAFLD. We employed RNA-seq and m1A-MeRIP-seq to identify key targets, followed by mechanistic validation of the YTHDF1–m1A–NUPR1 axis using biochemical, histological, and mRNA stability assays.

We identified a critical role for YTHDF1 in promoting hepatic steatosis. NUPR1, a stress-induced transcriptional regulator, undergoes m1A modification. YTHDF1 directly binds to m1A-modified NUPR1 mRNA, enhancing its stability, thereby leading to elevated NUPR1 protein levels. Functionally, upregulated NUPR1 acts as a core driver of NAFLD pathogenesis by activating lipogenic and suppressing fatty acid β-oxidation genes, thereby exacerbating hepatic lipid accumulation.

Our study unveils a novel epitranscriptomic mechanism in which YTHDF1, functioning as a dual-specificity reader, governs NAFLD progression through the m1A-NUPR1 axis. This not only expands the understanding of RNA modification recognition but also establishes the YTHDF1–m1A–NUPR1 pathway as a promising therapeutic target for metabolic liver disease.