This narrative review provides a detailed and comprehensive examination of hemoadsorption therapy and its role in treating severe poisoning. First, the global problem of suicidal and nonsuicidal self-injury is described, with regional differences in the types of poisons used noted. Lower- and middle-income countries are disproportionately affected by pesticides compared to high-income countries. Organophosphates often constitute the majority of pesticide poisoning in many of these countries. Next, we review the history of hemoadsorption therapy from its early origins to its current evolution. The key physical and chemical principles underlying extracorporeal therapy and its effectiveness are described. A review of the literature examining the evidence for the efficacy of hemoadsorption therapy in poisoning is presented. Current evidence-based guidelines are summarized, including toxin types, clinical indications, and the extracorporeal therapies recommended. Emerging evidence regarding the use of hemoadsorption therapy for severe organophosphate and calcium channel blocker poisoning is also considered. A care pathway for considering hemoadsorption in poisonings where formal guidelines are lacking is proposed. Both the hemoadsorption strategies used and the potential adverse effects of this therapy are discussed. For this narrative review, the PubMed/Medline was searched from inception to April 30, 2025, using the terms (“hemoperfusion” OR “hemadsorption”) AND (“poisoning”). Clinical trials, randomized controlled trials, and meta-analyses were included, along with additional relevant studies identified through a manual review of references. The role of modern resin bead hemoadsorption therapy for severe poisoning is expanding to include removal of commonly encountered poisons that are protein-bound and have a large volume of distribution. Using a multicycle approach, hemoadsorption therapy has shown improved outcomes for both calcium channel blockers and organophosphate poisoning.

Gastrointestinal (GI) cancers account for approximately one-third of annual cancer-related deaths globally, while outcomes remain poor despite advances in surgery, chemotherapy, radiotherapy, and immunotherapy. Given the challenges of persistent resistance and treatment-related toxicities in current therapies, the pivotal roles of the gut microbiota and fecal microbiota transplantation (FMT) in GI cancer therapy are increasingly recognized. This review aims to explore the potential and mechanisms of FMT as a therapeutic adjuvant in the treatment of GI cancers. FMT may enhance antitumor treatment efficacy and reduce treatment-related toxicity through multiple mechanisms, including enhancing antigen presentation, reshaping the tumor microenvironment, and preserving intestinal barrier function. Preliminary clinical evidence indicates that FMT combined with immune checkpoint inhibitors, chemotherapy, or radiotherapy can improve treatment response rates in some trials and may reverse resistance and alleviate associated intestinal toxicities in selected cases. However, clinical application is hindered by donor microbiota functional heterogeneity, substantial interindividual variability in engraftment, and the absence of validated predictive models. To advance FMT toward precision intervention, we propose a functional screening framework: the Healthy Donor-derived Microbiota Xenograft model as a preclinical functional screening platform and its subsequent clinical application, Xenograft-screened FMT, which links donor-level functional validation with personalized microbiota delivery. By integrating mechanistic insights, emerging preclinical and clinical evidence, and a functional screening framework, this review contributes to advancing FMT from an empirical intervention toward a precision adjuvant strategy and offers insights into future clinical investigation of FMT as a therapeutic approach in GI oncology.

Metabolic dysfunction–associated steatotic liver disease (MASLD) is increasing rapidly, yet regional differences in burden and care quality remain unclear. This study aimed to compare regional incidence, mortality, and disability; evaluate care quality; identify key determinants; and project future incidence.

We analyzed the Global Burden of Disease 2023 estimates of MASLD incidence, deaths, and disability-adjusted life years from 1990 to 2023 by age, sex, country, and region. Age-standardized rates were assessed using joinpoint regression. A composite Quality of Care Index (QCI) was derived through principal component analysis. Gradient boosting models with SHapley Additive exPlanations interpretation identified key predictors, and Bayesian age–period–cohort models generated incidence projections.

In 2023, South and East Asia had the largest numbers of new cases, while North Africa and the Middle East and Andean Latin America recorded the highest age-standardized incidence, mortality, and disability rates. Eastern Europe and Andean Latin America showed sustained increases in mortality and disability despite moderate incidence growth. QCI values were lowest in South Asia, Western Sub-Saharan Africa, and Eastern Europe. High body mass index and fasting plasma glucose were prominent contributors in comparative risk attribution analyses, and machine learning models identified age and calendar year as the strongest predictors of modeled burden patterns. Incidence is projected to continue increasing through 2050, particularly in India and China.

MASLD burden and care quality vary widely across regions. Low-QCI regions show higher mortality and disability, unfavorable metabolic risk profiles, and delayed detection patterns. Strengthening prevention, early case finding, fibrosis assessment, and treatment access may slow MASLD progression.

Ulinastatin, a broad-spectrum serine protease inhibitor widely used in Asia, has attracted increasing interest for its potential role in critical care. This review summarizes current evidence on its efficacy and safety in acute pancreatitis, severe acute pancreatitis, sepsis, acute respiratory distress syndrome, and perioperative management in cardiac surgery with cardiopulmonary bypass. Meta-analyses suggest that ulinastatin may improve outcomes by reducing mortality, shortening intensive care unit and hospital stays, and attenuating inflammatory responses. In severe acute pancreatitis, its use has been associated with reduced mortality and shorter hospitalization. In sepsis and septic shock, ulinastatin appears to lower all-cause mortality, decrease organ dysfunction scores, and reduce inflammatory markers. Evidence in acute respiratory distress syndrome indicates improvements in the oxygenation index and possible mortality reduction. Perioperative administration during cardiac surgery may mitigate postoperative inflammation and shorten the duration of mechanical ventilation. Despite these encouraging findings, most available studies originate from Asia and are limited by small sample sizes, heterogeneous designs, and inconsistent dosing regimens, which restrict generalizability and prevent standardized recommendations. Additionally, although ulinastatin demonstrates a favorable safety profile with a low incidence of adverse drug reactions, long-term and multinational pharmacovigilance data remain limited. Well-designed international, multicenter randomized controlled trials are required to clarify optimal dosing strategies, confirm clinical efficacy across diverse populations, and determine its independent effects compared with combination therapies. Overall, ulinastatin shows promise as a potential adjunctive therapy in critical care through modulation of inflammation and organ protection, but broader global adoption will depend on higher-quality evidence addressing current methodological gaps.

Nitric oxide (NO) is a crucial regulator of hepatic and systemic vascular tone. Abnormal distribution of NO in various anatomical locations is a pathogenetic characteristic of portal hypertension. Under normal portal pressure conditions, liver sinusoidal endothelial cells produce NO, which promotes both vasodilation and hepatic stellate cell relaxation. In portal hypertension, endothelial dysfunction, imbalance of asymmetric dimethylarginine levels, and production of superoxide result in impaired intrahepatic NO availability, leading to activation and contraction of hepatic stellate cells and worsening portal hypertension. Excess extrahepatic NO levels in the splanchnic vasculature result in systemic vasodilation, hyperdynamic circulation, and collateral vascular formation, worsening portal pressure. Abnormal clearance and production of NO can lead to extrahepatic complications, including hepatorenal syndrome and hepatopulmonary syndrome. Therapies including statins, phosphodiesterase-5 inhibitors, and midodrine have been developed to restore NO homeostasis but have achieved only partial success in modulating NO production, bioavailability, and distribution. The aim of this review is to update the understanding of the mechanisms and effects of NO dysregulation in cirrhosis as they relate to current and future therapeutic options.

The impact of baseline liver fibrosis severity on the effectiveness of pegylated interferon (Peg-IFN) combined with nucleos(t)ide analogs (NAs) in the treatment of hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) has not been fully clarified. This study aimed to investigate whether the effectiveness of this combination therapy differed according to the severity of baseline liver fibrosis.

A total of 172 HBeAg-positive CHB patients receiving Peg-IFN plus NAs were stratified according to non-invasive fibrosis markers (aspartate aminotransferase-to-platelet ratio index [APRI] and fibrosis-4 index [FIB-4]) into three groups: no significant fibrosis (n = 75), significant fibrosis (n = 70), and advanced fibrosis/cirrhosis (n = 27). The primary outcome was the HBeAg clearance rate at 24 months of treatment. Secondary outcomes included the hepatitis B surface antigen (HBsAg) clearance rate, the rate of HBsAg level decline > 1.0 log10, virological response, and improvement in non-invasive fibrosis indices.

At 24 months, HBsAg clearance and complete virological response rates were comparable across the three groups. Cumulative HBeAg clearance rates differed significantly (log-rank P = 0.027): 16.00%, 30.00%, and 40.74% in the three groups, respectively, with Group 3 higher than Groups 1 and 2. Multivariate analysis identified a significantly higher likelihood of HBeAg clearance in Group 3 versus Group 1 (adjusted odds ratio = 6.373, 95% confidence interval: 1.288–31.531, P = 0.023). Additionally, analysis of liver fibrosis outcomes showed that patients with more severe baseline fibrosis had a higher proportion of improvement in non-invasive fibrosis indices, with 95.00% in Group 3, while 42.98% of the overall cohort achieved fibrosis improvement.

Baseline fibrosis severity is associated with higher HBeAg clearance and greater improvement in non-invasive fibrosis indices during Peg-IFN plus NAs therapy in HBeAg-positive CHB.

Observational studies have shown that educational attainment is associated with the risk of myopia, but the causality of this relationship is unclear. The aim of the present study was to investigate the causal association between educational attainment and myopia.

Using publicly available data from genome-wide association studies, single nucleotide polymorphisms associated with educational attainment (college/university completion and years of education) were selected as instrumental variables. Causal associations with myopia risk were examined using two-sample Mendelian randomization (MR) analyses. Sensitivity analyses were conducted to assess the robustness of the results in terms of violations of MR assumptions.

The inverse variance–weighted analysis revealed potential causal associations of college/university completion (odds ratio (OR) = 1.102; 95% confidence interval (CI): 1.085–1.119; P < 0.001) and years of education (OR = 1.009; 95% CI: 1.007–1.010; P < 0.001) with myopia risk. MR-Egger and weighted median methods yielded similar results for both educational attainment measures.

MR evidence supports a potential causal association between educational attainment and myopia. This evidence highlights the need for careful management of myopia risk in individuals with higher educational attainment.

Apatinib has been shown to be efficacious in the treatment of gallbladder cancer. However, the underlying mechanisms remain unclear. This study aimed to explore pathways related to the antitumor effects of apatinib at the cellular level in gallbladder cancer.

NOZ and GBC-SD gallbladder cancer cells were treated with apatinib at concentrations of 0 μM, 10 μM, or 20 μM. The effect of apatinib on the proliferation of these cells was assessed using MTT and colony formation assays, and the effects of apatinib on cell cycle progression and DNA synthesis were evaluated using flow cytometry. Clinical cancer tissue samples, along with paired adjacent normal tissue samples, were obtained from 10 patients with gallbladder cancer. Immunohistochemistry, western blotting, and quantitative real-time polymerase chain reaction analyses were conducted to elucidate molecular changes induced by apatinib treatment.

Treatment with 20 μM apatinib significantly inhibited the expression of phosphorylated (p)-vascular endothelial growth factor receptor 2 (VEGFR2), p-AKT, and histone deacetylase 1 (HDAC1). Additionally, apatinib treatment led to upregulated expression of p-cyclin-dependent kinase 1, p21, and Bax, and downregulated expression of cell division cycle 25B, B-cell lymphoma 2, Snail, and Slug. Apatinib decelerated DNA replication and induced cell cycle arrest at the G2/M phase, consequently suppressing the proliferation of gallbladder cancer cells.

Apatinib inhibits the proliferation of gallbladder cancer cells, and the mechanism involves VEGFR2/AKT, HDAC1, and downstream genes. These findings provide a basis for further investigation into the molecular mechanisms underlying the inhibitory effect of apatinib in gallbladder cancer.

Given that hemodynamic fluctuations acutely escalate the risk of devastating rebleeding and secondary neurological deficits in unsecured ruptured intracranial aneurysms, this study aimed to synthesize the best available evidence for blood pressure management in this population and to provide an evidence-based foundation for clinical nursing practice.

A systematic search was conducted in domestic and international databases and relevant websites for evidence pertaining to blood pressure management in patients with ruptured intracranial aneurysms, including clinical practices, guidelines, expert consensuses, evidence summaries, and systematic reviews/meta-analyses. The search period covered database inception up to June 2025. Two researchers independently performed literature quality assessments and evidence extraction, with particular attention to nursing-relevant evidence on hemodynamic monitoring, bedside assessment, complication prevention, fluid management, and follow-up coordination.

A total of 17 studies were included, comprising 11 guidelines, 4 expert consensuses, and 2 clinical decision entries. The synthesized evidence yielded 32 recommendations, structured into 6 core clinical domains: personnel and environmental configuration, individualized blood pressure targeting, precision hemodynamic monitoring, complication prevention, fluid therapy strategy, and longitudinal follow-up protocols. These recommendations further clarified key nursing responsibilities in triage coordination, continuous blood pressure surveillance, neurological assessment, delayed cerebral ischemia surveillance, fluid balance monitoring, and long-term follow-up.

Blood pressure management in patients with ruptured intracranial aneurysms should be individualized and multidisciplinary. The synthesized evidence highlights key nursing priorities in hemodynamic monitoring, delayed cerebral ischemia surveillance, fluid management, and follow-up coordination, and may inform standardized clinical nursing protocols.