Atrial fibrillation and chronic kidney disease (CKD) frequently coexist, increasing thromboembolic and bleeding risks. This is a narrative review of pathophysiology and clinical evidence for anticoagulation strategies in CKD patients. Direct oral anticoagulants are preferred in CKD stages 1–4. Recent data suggest that the efficacy of apixaban and rivaroxaban is comparable to that of warfarin in end-stage renal disease. In advanced CKD, anticoagulation should be tailored with close monitoring.

Dysregulated lipid metabolism contributes to hepatocellular carcinoma (HCC) progression, but the prognostic value and mechanistic roles of lipid metabolism-related long noncoding RNAs (LRLs) remain insufficiently characterized. This study aimed to construct and validate an LRL-based prognostic model and to investigate the biological function and metabolic mechanism of AC026412.3 in HCC.

Transcriptomic and clinical data from the The Cancer Genome Atlas Liver Hepatocellular Carcinoma cohort were analyzed to identify LRLs based on their correlation with curated lipid metabolism genes. Differential expression, univariate Cox, least absolute shrinkage and selection operator (LASSO), and multivariate Cox analyses were performed to construct a prognostic signature, which was evaluated using Kaplan–Meier survival and time-dependent receiver operating characteristic (ROC) analyses. Functional enrichment analyses Gene Ontology [GO], Kyoto Encyclopedia of Genes and Genomes [KEGG] and gene set enrichment analysis [GSEA], mutation profiling, tumor mutational burden, immune infiltration estimation, and consensus clustering were applied to characterize associated features. A key LRL was identified through integrated bioinformatic screening and prioritization. Its biological role was assessed by quantitative reverse transcription polymerase chain reactionq (RT-PCR), western blotting, BODIPY staining, colony formation, Transwell assays, and xenograft models. RNA sequencing followed by pathway enrichment analysis was conducted to explore underlying mechanisms.

A three-LRL signature (AL031985.3, NRAV, and AC026412.3) stratified HCC patients into distinct risk groups with significantly different survival outcomes and demonstrated independent prognostic value. AC026412.3 was markedly upregulated in HCC and associated with poor prognosis. Functional assays demonstrated that AC026412.3 promoted proliferation, invasion, and tumor growth while reducing lipid accumulation. Mechanistically, AC026412.3 upregulated solute carrier family 22 member 5 (SLC22A5), enhanced fatty acid β-oxidation, and increased adenosine triphosphate (ATP) production, thereby driving metabolic reprogramming.

This study establishes a robust LRL-based prognostic model and identifies AC026412.3 as a key regulator of lipid metabolic reprogramming via the SLC22A5–fatty acid β-oxidation axis, highlighting its potential as a biomarker and therapeutic target in HCC.

Ferroptosis, an iron-dependent form of regulated cell death, serves as an important mechanism associated with cancer progression. Natural compounds, particularly alkaloids, have emerged as attractive candidates for regulating ferroptotic cell death, thereby providing a promising anticancer strategy. However, the molecular mechanisms underlying their antitumor effects remain poorly understood. In this study, we aimed to investigate the antitumor effects and underlying mechanisms of natural alkaloids against hepatocellular carcinoma (HCC).

An alkaloid library was used to screen alkaloids with anti-HCC activity. A combination of proteomic profiling, in vitro functional assays, and in vivo animal experiments was performed to explore the biological roles and molecular mechanisms of the lead compound.

Through high-throughput screening of an alkaloid library, we identified palmatine (PAL), an active component isolated from Fibraurea recisa Pierre, as a potential ferroptosis sensitizer in HCC cells. PAL treatment triggered typical ferroptotic features in HCC cells, including elevated ferrous iron, reactive oxygen species, and lipid peroxidation, along with decreased glutathione levels. Importantly, the pro-ferroptotic effect of PAL was significantly abolished by two ferroptosis inhibitors, ferrostatin-1 and deferoxamine. Mechanistically, PAL directly interacted with troponin T1 (TNNT1) to trigger its K48-linked polyubiquitination and subsequent protein degradation. Ectopic TNNT1 overexpression significantly rescued PAL-mediated ferroptosis and abrogated its tumor-suppressive effects. In vivo animal models further confirmed that PAL suppressed tumor growth by downregulating TNNT1, with a favorable safety profile.

This study reveals a previously unrecognized role of PAL as a ferroptosis sensitizer and highlights its translational potential for anti-HCC therapy.

Biliary atresia (BA) is a severe pediatric cholangiopathy characterized by rapidly progressive liver fibrosis. This study aimed to characterize scar-associated macrophages and investigate the role of plasminogen (PLG)–plasminogen receptor with a C-terminal lysine (PLGRKT) signaling in BA-associated fibrogenesis.

Single-cell RNA sequencing and spatial transcriptomics were applied to liver tissues from patients with BA and non-BA controls. Key findings were validated in an independent cohort using quantitative polymerase chain reaction and multiplex immunohistochemistry. The functional role of the PLGRKT pathway was further examined using primary human peripheral blood mononuclear cell-derived macrophages with small interfering RNA (siRNA)-mediated PLGRKT knockdown, together with co-culture systems involving LX-2 hepatic stellate cells and human liver organoids. In vivo therapeutic potential was evaluated in a murine bile duct ligation model of cholestatic liver fibrosis using macrophage-targeted Plgrkt–Trem2 antibody–siRNA conjugates.

In BA, scar-associated macrophages (SAMs) increased with fibrosis progression and co-localized with hepatic stellate cells in fibrotic areas. PLGRKT was upregulated in BA liver tissue and increased during monocyte-to-macrophage differentiation. In primary human macrophages, PLG induced a PLGRKT-dependent pro-fibrotic phenotype, and conditioned medium from these cells increased COL1A1 deposition in hepatic stellate cells and human liver organoids. In vivo, macrophage-targeted Plgrkt–Trem2 antibody–siRNA conjugates reduced SAM accumulation and attenuated bile duct ligation-induced liver fibrosis.

These findings support a role for SAMs and the PLGRKT–SAM axis in BA-associated liver fibrosis and suggest that PLGRKT warrants further investigation as a potential macrophage-directed anti-fibrotic target.

Head, thoracic, abdominal, and pelvic polytrauma is clinically complex and requires coordinated multidisciplinary care, creating an urgent need for standardized guidance. This guideline aims to provide an evidence-based foundation and clinical pathway for the diagnosis, assessment, damage control, surgical timing, and acute-phase management of patients with head, thoracic, abdominal, and pelvic polytrauma. Led by the Senior Department of Neurosurgery, Chinese PLA General Hospital, a multidisciplinary working group comprising experts in thoracic surgery, general surgery, orthopedics, critical care medicine, anesthesiology, radiology, emergency medicine, nursing, and related disciplines developed the guideline through systematic review of the relevant literature, consideration of the characteristics of trauma care in China’s military and civilian medical systems, and two rounds of expert voting and consensus decision-making. The guideline addresses 22 key clinical questions covering imaging assessment, damage-control resuscitation, prioritization of craniocerebral and torso injury management, anticoagulation and hemostatic management, intensive care, and early rehabilitation. A total of 22 recommendations were formulated by integrating evidence quality, clinical feasibility, and implementability, together with corresponding implementation points and quality-control indicators. The guideline emphasizes stabilization of vital signs, damage-control principles, multidisciplinary collaboration, standardized clinical pathways, and a tiered trauma-care system. Implementation of these recommendations may improve the consistency and timeliness of multidisciplinary care and provide a framework for reducing early mortality while preserving neurological and functional outcomes.

Biliary atresia (BA) is the leading cause of pediatric obstructive cholestasis and a major indication for liver transplantation in infants. Organoid models are increasingly used to investigate BA pathogenesis and therapeutic responses, but incomplete methodological and clinical reporting may limit cross-study comparison and translational interpretation. This study aimed to map the landscape of BA-related organoid research, identify major reporting gaps, and propose the Biliary Atresia Minimum Reporting Standard (BA-MRS) as a preliminary framework for improving reporting completeness.

PubMed, Scopus, and Web of Science Core Collection were searched on March 8, 2026, in accordance with the PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews) and the 2024 Joanna Briggs Institute (JBI) Manual for Evidence Synthesis. Reporting completeness was assessed using a 36-item BA-MRS across six domains, scored as fully reported, partially reported, not reported, or not applicable.

Twenty-six studies published between 2020 and 2026 were included. Fibrosis and epithelial–mesenchymal transition were the most frequently studied themes, whereas only one study linked organoid findings to post-Kasai outcomes. BA case/model definition, ethics approval, and differentiation protocols were fully reported in all applicable studies (100%). In contrast, contamination monitoring (3.8%), core biliary function assays (34.6%), and clinical outcome linkage (26.3%) were poorly reported. Culture System and Sample Acquisition showed the lowest domain-level fully reported rates (58.1% and 63.2%, respectively).

BA organoid research has progressed beyond early model development, but reporting remains insufficient for robust comparison, reproducibility, and clinically meaningful interpretation. BA-MRS may serve as a preliminary framework for improving standardized reporting in future studies.

Biliary duct invasion (BDI) is an underrecognized growth pattern of colorectal cancer (CRC) liver metastases that can mimic intrahepatic cholangiocarcinoma or intraductal papillary neoplasm of the bile duct. Its prevalence and clinicopathologic associations remain unclear. This study aimed to determine the prevalence of BDI and its clinicopathologic associations in surgically resected CRC liver metastases.

We retrospectively analyzed 133 consecutive patients who underwent hepatic resection for CRC liver metastases. Clinicopathologic variables, including age, sex, resection type, tumor differentiation, lymphovascular invasion (LVI), tumor budding, surgical margin status, and primary tumor characteristics, were compared between BDI-positive and BDI-negative cases. Categorical variables were analyzed using the chi-square, Fisher exact, or Fisher-Freeman-Halton exact test, as appropriate; continuous variables were analyzed using the Mann-Whitney U test.

BDI was identified in 19 of 133 cases (14.3%). Male sex showed the strongest numerical trend toward BDI (84.2% vs. 61.4%, P = 0.096), and LVI showed a nonsignificant numerical trend toward higher BDI rates (26.3% vs. 12.3%, P = 0.149). No clinicopathologic variable in the primary cohort analysis reached statistical significance after Bonferroni correction (α = 0.0050).

BDI occurs in approximately 14% of surgically resected CRC liver metastases in this cohort. Male sex and LVI show nonsignificant numerical trends toward higher BDI rates, but these findings should be interpreted cautiously given the limited sample size. Accurate histopathologic recognition of BDI and its distinction from intrahepatic cholangiocarcinoma remain important for correct pathologic diagnosis. Further prospective studies are warranted to clarify the clinicopathologic and prognostic significance of BDI.