Extensive burn injuries are associated with a profound systemic response, the severity of which increases with the extent of tissue damage. Beyond local destruction, extensive burns induce a sustained immune-inflammatory disturbance that alters immune regulation and contributes to secondary organ failure and infectious complications. These mechanisms are major determinants of adverse outcomes in critically ill patients with burns. In this context, therapeutic strategies targeting immune dysregulation have gained increasing attention. Immunomodulatory approaches aim to limit excessive inflammatory signaling while maintaining effective host defense. Among extracorporeal blood purification techniques, hemoadsorption has emerged as a potential adjunctive therapy designed to reduce circulating inflammatory mediators, particularly cytokines, and to attenuate systemic inflammatory burden. Rather than providing another general overview of extracorporeal blood purification, this review focuses specifically on the cellular and mechanistic basis of burn-induced immune dysregulation and offers a stratified, critical appraisal of the experimental and clinical evidence for hemoadsorption in burns, together with current safety considerations and unresolved questions that should guide future research. Experimental studies and early clinical observations suggest that hemoadsorption may contribute to hemodynamic stabilization and modulation of inflammation in critically ill patients, including those with severe burns. However, clinical evidence in this specific population remains scarce, and its impact on patient-centered outcomes has not yet been established. Although available data suggest that this technique is generally well tolerated, the non-selective removal of circulating molecules underscores the need for careful patient selection and close monitoring. Future investigations should focus on defining the appropriate indications, optimal timing, and treatment duration of hemoadsorption for burn care. Comparative studies with other immunomodulatory strategies are required to clarify its role within the therapeutic armamentarium for burn-induced immune dysfunction.

Human serum albumin (HSA) is a multifunctional carrier protein that helps maintain vascular barrier integrity and intravascular fluid homeostasis and has long been used in the management of critically ill patients, including those with acute brain injury. HSA is thought to exert neuroprotective effects through four complementary mechanisms: oncotic/volume expansion and hemodilution, antioxidant and anti-inflammatory effects, HSA-nitric oxide-mediated antithrombotic activity, and glycocalyx stabilization, although the precise pathways remain incompletely understood. Despite its biological rationale, the clinical efficacy of HSA in severe neurological disorders remains inconclusive, and few guidelines provide specific recommendations for its use in neurological care. This uncertainty stems primarily from the complex etiology and heterogeneous pathophysiology of neurological disorders, as well as inconsistent findings across existing studies. This narrative review aims to summarize the current evidence on HSA use in traumatic brain injury, acute ischemic stroke, and aneurysmal subarachnoid hemorrhage, identify existing knowledge gaps, and provide insights for future research and clinical practice. We screened records from PubMed, Embase, the Cochrane Library, CNKI, and Yiigle, as well as ClinicalTrials.gov, ChiCTR, and ChinaDrugTrials. A total of 29 human and animal studies were included. Collectively, available evidence supports a biological rationale for HSA therapy in neurocritical care, yet its clinical benefit remains incompletely established and substantial challenges persist. Prospective randomized controlled trials are warranted to clarify the efficacy and safety of HSA and determine whether preliminary encouraging findings can inform standardized guidelines and expert consensus recommendations, particularly regarding optimal concentration, timing, and patient selection.

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.

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.

The IMbrave050 trial suggested that adjuvant immune checkpoint inhibitor therapy may benefit patients with hepatocellular carcinoma exceeding the “up-to-7” criterion. This study aimed to compare survival outcomes and safety between such patients receiving adjuvant programmed cell death protein 1 inhibitors and those undergoing active surveillance after curative resection.

Data were prospectively collected from patients at 13 medical centers in China between 2019 and 2024. The study was designed according to a target trial emulation framework, and propensity score matching was used to reduce confounding. The primary endpoint was recurrence-free survival; secondary endpoints included overall survival and incidence of treatment-related adverse events.

Median follow-up was 32.7 months (interquartile range, 20.9–47.5). Propensity score matching yielded 200 patients per group. Median recurrence-free survival was longer in the adjuvant group (28.0 months; 95% confidence interval [CI], 21.7–34.3) than in the surveillance group (14.4 months; 95% CI, 10.7–18.1; hazard ratio, 0.58; 95% CI, 0.45–0.74). Median overall survival was not reached in the adjuvant group and was 45.0 months (95% CI, 37.8–52.1) in the surveillance group (hazard ratio, 0.63; 95% CI, 0.45–0.89). The most frequent grade 3–4 treatment-related adverse events were hand–foot skin reaction (7.2%), elevated alanine aminotransferase (5.8%), and elevated aspartate aminotransferase (5.3%).

Adjuvant programmed cell death protein 1 inhibitors, with or without molecularly targeted agents, were associated with longer recurrence-free survival and acceptable safety in patients with hepatocellular carcinoma exceeding the “up-to-7” criterion.

CXC chemokine receptor 2 (CXCR2) expression has been observed in normal neuroendocrine cells, but its role in neuroendocrine neoplasms is less well established. We aimed to evaluate CXCR2 expression with somatostatin receptor type 2 (SSTR2) expression in pancreatic neuroendocrine tumors (PanNETs) and small intestinal neuroendocrine tumors (SI-NETs).

This was a cross-sectional study. Pathology archives were searched for PanNETs with ≥2 resected liver metastases and SI-NETs with resected liver metastases, mesenteric tumor deposits (MTDs), and/or peritoneal metastases. Immunohistochemistry for CXCR2 was performed on de-identified tissue microarrays containing PanNETs and SI-NETs. SSTR2 and CXCR2 immunohistochemistry was also performed on tumor blocks from primary and metastatic PanNETs and SI-NETs. Based on H-scores, expression was scored as negative (<50), weak (50–100), moderate (>100–200), or strong (>200). Marker expression was descriptively reported among primary tumors, liver metastases, MTDs, and peritoneal metastases.

Among 12 primary PanNETs and 38 liver metastases, mean CXCR2 H-scores were 269.6 ± 36.7 and 254.6 ± 75.5, respectively, and mean SSTR2 H-scores were 261.5 ± 61.9 and 259.3 ± 70.9, respectively. All 84 SI-NET lesions showed moderate/strong CXCR2 expression, whereas 12 showed negative/weak SSTR2 expression. CXCR2 H-scores were 284.0 ± 26.5 in primary tumors, 272.5 ± 28.7 in MTDs, 269.6 ± 42.8 in liver metastases, and 265.0 ± 51.5 in peritoneal metastases. SSTR2 expression appears to be lower in MTDs than in primary tumors (182.2 ± 76.5 vs 235.9 ± 55.9).

CXCR2 is moderately/strongly expressed in most sampled PanNETs and all sampled SI-NETs. In SI-NETs, moderate/strong CXCR2 expression is less heterogeneous than SSTR2 expression.

Fuzheng Huayu, a patent herbal product, has shown promise in liver fibrosis and cirrhosis. The effect of Fuzheng Huayu on portal hypertension due to cirrhosis and the consequent complications needs further investigation. In this study, we aimed to evaluate the association of adjunctive Fuzheng Huayu plus entecavir with liver-related events and variceal regression in patients with compensated HBV-related cirrhosis.

A post hoc analysis was conducted using data from two randomized controlled trials implemented at eight clinical centers in China (ClinicalTrials.gov numbers: NCT02945982; NCT02945956). Patients with compensated hepatitis B virus-related cirrhosis were enrolled from October 2017 to March 2021. The primary endpoint was a composite of liver events and the individual components, including variceal bleeding, ascites, overt hepatic encephalopathy, and hepatocellular carcinoma.

A total of 218 participants (Fuzheng Huayu group: 110 and control group: 108; mean age, 51.5 years; 66.5% male; median observational follow-up time, 23.1 months) were included in the primary analysis. The occurrence of total liver events was less frequent in the Fuzheng Huayu group than in the control group (hazard ratio = 0.408 [0.187–0.892], P = 0.020). Among the individual components of liver events, the incidence of ascites was significantly lower in the Fuzheng Huayu group than in the control group (1.8% vs. 9.3%, P = 0.016). In addition, the rate of variceal regression was significantly higher in the Fuzheng Huayu group (27.3% vs. 10.2%, P < 0.001). Finally, there were no significant differences in the occurrence of adverse events between the two groups.

In this post hoc analysis of two randomized controlled trials, adjunctive Fuzheng Huayu plus entecavir was associated with fewer liver-related events, particularly ascites, and a higher rate of variceal regression than entecavir alone in patients with compensated hepatitis B virus-related cirrhosis. These findings warrant confirmation in adequately powered prospective studies.

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.