Endovascular embolization is a cornerstone treatment for intracranial aneurysms, and transfemoral access (TFA) has traditionally been the default vascular route. Transradial access (TRA) is increasingly used in neurointervention because it may reduce clinically important access-site complications, improve postprocedural comfort, and facilitate earlier ambulation. This narrative review aims to summarize direct and indirect evidence comparing TRA and TFA for intracranial aneurysm embolization, with attention to technical feasibility, access conversion, puncture-site complications, neurological events, radiation exposure, procedure duration, recovery, and cost considerations. Direct comparative evidence specific to aneurysm embolization remains limited and is mainly observational; some supporting data come from diagnostic cerebral angiography, mixed therapeutic neurointervention, and cardiovascular access literature. Available data suggest that TRA may be a safe and feasible option for selected patients when performed by experienced operators, particularly when radial anatomy is favorable and the intended device strategy is compatible with upper-extremity access. TFA remains essential for complex anatomy, large-bore device requirements, or insufficient TRA expertise. Access selection should therefore be individualized rather than based on a presumption of universal superiority. Well-designed multicenter studies are needed to define aneurysm-specific outcomes, long-term angiographic durability, patient-reported outcomes, and cost-effectiveness.

Esophageal adenocarcinoma (EAC) and gastric cancer (GC) remain major causes of cancer-related mortality worldwide, largely because of late-stage diagnosis. Barrett’s esophagus (BE) is the established precursor setting for EAC, whereas gastric intestinal metaplasia is an important precursor lesion in the intestinal-type gastric carcinogenesis pathway. Aberrant DNA methylation arises early in both pathways and may offer greater sensitivity and specificity than histology or serology alone, while also illuminating the biology of neoplastic progression. This review evaluates the evidence and translational potential of DNA methylation biomarkers in upper gastrointestinal adenocarcinoma.

PubMed, Web of Science, and EMBASE were searched for studies published before May 2026 addressing DNA methylation biomarkers in BE, EAC, gastric intestinal metaplasia, and GC. Tissue-based, minimally invasive, and circulating biomarkers were reviewed, with emphasis on diagnostic performance, progression risk, biological significance, and clinical translation.

Methylation alterations accumulate during progression from precancerous lesions to invasive cancer and distinguish disease states in tissue and minimally invasive specimens. Methylation-based assays show promising diagnostic performance in BE and EAC, including nonendoscopic cytology-based approaches and risk-stratification assays, and circulating methylated DNA shows potential for noninvasive detection of EAC and GC. However, heterogeneity in populations, specimens, assay platforms, and study designs, together with limited prospective validation, remains a barrier to implementation.

The field is moving rapidly from discovery toward practice: Cytosponge-TFF3 with biomarker panels has been evaluated in real-world UK surveillance pathways, the EsoCheck/EsoGuard methylation assay is clinically available, and Esopredict is the first epigenetic prognostic assay clinically validated to risk-stratify BE, while multicancer early detection assays undergo prospective evaluation. Multicenter studies of clinical utility and cost-effectiveness remain the decisive step before routine adoption.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly prevalent worldwide and is frequently encountered in patients undergoing liver transplantation and hepatic surgery. Although hepatic steatosis was once considered a relatively benign condition, accumulating evidence indicates that MASLD is associated with reduced tolerance to ischemic stress and increased susceptibility to ischemia–reperfusion injury, which may contribute to graft dysfunction and postoperative liver injury. In this mini review, we used the concept of hepatic resilience, referring to the ability of the liver to maintain homeostasis during stress and recover after injury. We discussed how MASLD may reduce hepatic resilience through mechanisms involving lipotoxicity, mitochondrial dysfunction, oxidative stress, inflammatory activation, regulated cell death, and impaired regeneration. MASLD represents a heterogeneous disease spectrum, and susceptibility to ischemia–reperfusion injury may differ according to disease stage and phenotype, particularly in the presence of progressive inflammation and fibrosis. We further summarized strategies aimed at improving hepatic resilience, including metabolic optimization, mitochondrial protection, modulation of reperfusion-associated inflammation, and enhancement of tissue repair. However, current evidence remains limited by the paucity of human studies and validated approaches for assessing hepatic resilience. Further investigation of these mechanisms may help develop individualized strategies to protect the liver in patients with MASLD during hepatic surgery and transplantation.

The huge burden of type 1 diabetes mellitus (T1DM) has been a source of concern globally since the Industrial Revolution in the 18th–19th centuries. To this end, studies have shown that certain environmental changes that accompanied the Revolution may have increased the risk and burden of the disease in genetically predisposed individuals. However, documented studies that synthesize these environmental triggers are scarce. As a result, the current study was conceived to synthesize the environmental triggers of T1DM to boost public awareness. Relevant information was retrieved from reputable academic databases; namely, Scopus, PubMed, SpringerLink, and Embase. The results showed that chemical exposure, viral infection, gut microbiome disruption, vitamin and mineral deficiencies, inadequate or exclusive breastfeeding, as well as early exposure to infant feeding formulas could increase the risk and burden of T1DM in genetically predisposed individuals. As a consequence, these triggers could compromise the expression of certain genes involved in insulin synthesis and immune function, such as the human leukocyte antigen (HLA), insulin (INS), cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), and protein tyrosine phosphatase non-receptor type 22 (PTPN22) genes. This would result in a dysfunctional immune system in which immune cells, such as T-cells and B-cells and molecules, such as cytokines would attack self-tissues, thus causing autoimmunity of the pancreatic beta cells. Environmental triggers could also induce the T1DM pathophysiology by modifying the epigenome of the mentioned genes. Furthermore, some epigenetic changes could be reversed, which would infer that treatment procedures that would include the pathophysiology of the environmental triggers could be more effective.

Emerging evidence suggests that RNA-binding motif (RBM) proteins are involved in hepatocarcinogenesis and act either as oncogenes or tumor suppressors. The objective of this study was to investigate the role of RBM34, an RBM protein, in hepatocellular carcinoma (HCC).

We first examined the expression of RBM34 across cancers. The correlation of RBM34 with clinicopathological features and the prognostic value of RBM34 for HCC was then investigated. Functional enrichment analysis of RBM34-related differentially expressed genes (DEGs) was performed to explore its biological function. RNA sequencing (RNA-seq) was applied to identify downstream genes and pathways affected upon RBM34 knockout. The correlation of RBM34 with immune characteristics was also analyzed. The oncogenic function of RBM34 was examined in in vitro and in vivo experiments.

RBM34 was highly expressed in hepatocellular carcinoma and correlated with poor clinicopathological features and prognosis. RBM34 was positively associated with tumor immune cell infiltration, biomarkers of immune cells, and immune checkpoint expression. A positive correlation was also observed between RBM34, T cell exhaustion, and regulatory T cell marker genes. Knockout of RBM34 significantly inhibited cell proliferation, migration, and xenograft tumor growth, and sensitized HCC cells to sorafenib treatment. RBM34 inhibition reduced FGFR2 expression and affected PI3K-AKT pathway activation in HCC cells.

Our study suggests that RBM34 may serve as a new prognostic marker and therapeutic target of HCC.

Naringenin is an anti-inflammatory flavonoid that has been studied in chronic liver disease. The mechanism specific to its antifibrosis activity needs further investigation This study was to focused on the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) pathway in hepatic stellate cells and clarified the antifibrosis mechanism of naringenin.

The relationship between the cGAS-stimulator of interferon genes (STING) pathway and liver fibrosis was analyzed using the Gene Expression Omnibus database. Histopathology, immunohistochemistry, fluorescence staining, Western blotting and polymerase chain reaction were performed to assess gene and protein expression levels associated with the cGAS pathway in clinical liver tissue samples and mouse livers. Molecular docking was performed to evaluate the relationship between naringenin and cGAS, and western blotting was performed to study the expression of inflammatory factors downstream of cGAS in vitro.

Clinical database analyses showed that the cGAS-STING pathway is involved in the occurrence of chronic liver disease. Naringenin ameliorated liver injury and liver fibrosis, decreased collagen deposition and cGAS expression, and inhibited inflammation in carbon tetrachloride (CCl4)-treated mice. Molecular docking found that cGAS may be a direct target of naringenin. Consistent with the in vivo results, we verified the inhibitory effect of naringenin on activated hepatic stellate cells (HSCs). By using the cGAS-specific agonist double-stranded (ds)DNA, we showed that naringenin attenuated the activation of cGAS and its inflammatory factors affected by dsDNA. We verified that naringenin inhibited the cGAS-STING pathway, thereby reducing the secretion of inflammatory factors by HSCs to ameliorate liver fibrosis.

Interrupting the cGAS-STING pathway helped reverse the fibrosis process. Naringenin has potential as an antihepatic fibrosis drug.