The pathogenic role of MIR142 genetic abnormalities in the development of primary diffuse large B-cell lymphoma (DLBCL) of the central nervous system (CNS) is unexplored. The objective of this study was to investigate the frequency, spectrum, and functional significance of mutations in the MIR142 gene in primary CNS DLBCL.

Direct Sanger sequencing of the MIR142 gene was performed in tumor tissue from 35 patients with primary DLBCL of the CNS. In silico prediction of microRNA (miRNA)–target interactions, enrichment analysis of target gene ontologies, and prediction of the secondary structure and minimum free energy of the miRNA hairpin were performed.

The mutation frequency was 37.1% (95% confidence interval: 23.2–53.7%). The vast majority of the identified single-nucleotide variants were located outside the regions encoding mature miRNA chains. In silico analysis showed that the n.29A>G mutation located in the seed sequence of miR-142-5p resulted in a significant reduction in the number of potential targets and alterations to the interaction spectrum. All single-nucleotide variants identified in the study patients caused a change in minimum free energy and affected the shape and length of the hairpin stem of pri-miRNA. The results indicate the fragility of the pri-miR-142 hairpin.

The frequency of gene mutations in primary DLBCL of the CNS significantly exceeds that reported for systemic DLBCL.

Immunothrombosis, the interplay between immune activation and coagulation, contributes to disease progression in inflammatory disorders. Its role in hepatitis B virus–related acute-on-chronic liver failure (HBV-ACLF) and the involvement of neutrophil extracellular traps (NETs) remain unclear. This study aimed to elucidate NETs-mediated immunothrombosis in HBV-ACLF.

Liver single-cell RNA sequencing data from HBV-ACLF patients and healthy controls were analyzed to define immune and endothelial transcriptional profiles. A cohort of 46 HBV-ACLF patients, 20 chronic hepatitis B patients, and 20 healthy controls was assessed for circulating NETs, endothelial injury markers, and coagulation parameters. Histopathology and in vitro assays examined NETs distribution and endothelial interactions.

NETs were markedly elevated in HBV-ACLF and correlated with endothelial injury markers (syndecan-1, von Willebrand factor, soluble thrombomodulin), coagulopathy, and prognostic scores. Histology revealed NETs colocalization with endothelial cells and platelets within hepatic microthrombi. NETs from patient neutrophils impaired endothelial integrity and enhanced procoagulant activity in vitro. Mechanistically, toll-like receptor 2 (TLR2) and complement component 5a receptor 1 (C5aR1) signaling were involved in NETs formation, and their pharmacological inhibition reduced NETs generation.

NETs are associated with endothelial injury and immunothrombosis in HBV-ACLF. Mechanistic analyses suggest a role for TLR2 and C5aR1 pathways in NETs formation, indicating potential targets for future therapeutic investigation.

Hepatic ischemia–reperfusion (HIR) injury impairs outcomes post–liver transplantation. Therefore, we aimed to investigate the role and mechanism of miR-381-3p in HIR.

The study enrolled 150 healthy controls, 82 non-HIR-injured patients, and 68 patients with HIR injury following liver transplantation. Clinical data were analyzed. Multivariate analysis identified HIR risk factors; the predictive value of miR-381-3p was assessed via receiver operating characteristic analysis. An in vitro hypoxia/reoxygenation (H/R) model was established and employed. The cellular effects of miR-381-3p and JAK2 were evaluated using CCK-8, flow cytometry, ELISA, luciferase, RIP, and bioinformatics.

Serum miR-381-3p was significantly elevated in HIR compared with the other groups. miR-381-3p was the strongest independent HIR risk factor, which was confirmed by receiver operating characteristic analysis. H/R upregulated miR-381-3p. Inhibiting miR-381-3p counteracted H/R-induced decreased viability and increased apoptosis, inflammation, and oxidative stress. miR-381-3p directly bound to and suppressed JAK2 via its 3′ untranslated region (validated by luciferase and RIP). Transfection of si-JAK2 abolished the protective effects of miR-381-3p inhibition.

miR-381-3p exacerbates post-transplant HIR by directly targeting JAK2, amplifying inflammation and oxidative stress. Thus, our findings nominate serum miR-381-3p as a promising non-invasive biomarker and suggest its potential as a therapeutic target for mitigating HIR injury.

Thyroid nodules are increasingly detected in clinical practice, and accurate imaging evaluation is essential for risk stratification, treatment planning, and postoperative surveillance of thyroid cancer. Although ultrasound remains the first-line modality for thyroid nodule assessment, the roles of computed tomography (CT), spectral CT, magnetic resonance imaging (MRI), and positron emission tomography-computed tomography (PET-CT) vary across clinical scenarios, and the optimal integration of these modalities remains insufficiently standardized. In particular, existing studies often focus on individual imaging techniques, while practical guidance on modality selection for initial screening, preoperative anatomical assessment, recurrence monitoring, and high-risk disease evaluation remains limited. This narrative review summarizes the imaging principles, clinical indications, diagnostic value, advantages, and limitations of ultrasound, CT, spectral CT, MRI, and PET-CT in the evaluation of thyroid nodules and thyroid cancer. Future advances should focus on standardized multimodal imaging strategies, quantitative functional imaging, radiomics, and carefully validated artificial intelligence-assisted approaches to improve individualized diagnosis and management of thyroid nodules and thyroid cancer.

Post-stroke dysphagia management research has primarily focused on screening, assessment, and intervention strategies, with limited objective indicators for evaluating nursing care quality. This study aimed to develop a dysphagia nursing quality evaluation index system for neurosurgical inpatients with stroke.

Using the “structure-process-outcome” three-dimensional quality model as the theoretical framework, a preliminary quality evaluation index system was constructed through literature analysis and group discussion. A two-round Delphi expert consultation was conducted among 25 purposively selected clinical experts from tertiary Class A hospitals, with inclusion criteria requiring a bachelor’s degree or higher, an intermediate professional title or above, and at least 10 years of clinical experience in stroke nursing or related fields. The analytic hierarchy process was used to determine indicator weights. Outcome measures included expert authority coefficients (Cr), Kendall’s W concordance coefficient, internal consistency reliability (Cronbach’s α), and the final indicator structure.

The Cr values were 0.87 and 0.88 across the two rounds. Kendall’s W concordance coefficient increased from 0.207 to 0.235 (P < 0.001), indicating statistically significant expert agreement. The final index system comprised 3 first-level indicators, 11 second-level indicators, and 44 third-level indicators, with all indicator definitions and weights determined. The overall Cronbach’s α was 0.86, indicating preliminary internal consistency.

This study developed a dysphagia nursing quality evaluation index system for neurosurgical inpatients with stroke using the three-dimensional quality model and the Delphi method. The system showed acceptable expert authority, statistically significant expert agreement, and preliminary internal consistency, suggesting potential applicability for nursing quality monitoring in neurosurgical wards and Neurosurgery Intensive Care Units. Further clinical validation is needed before routine implementation.

Extrahepatic cancers have been recognized as a significant outcome of metabolic dysfunction–associated steatotic liver disease (MASLD), which involves five cardiometabolic risk factors, including hypertension, and is associated with the tumorigenesis of several cancers or with anti-cancer treatment. We aimed to investigate the association between hypertension, liver fibrosis, and extrahepatic cancers in the MASLD population.

This multicenter cross-sectional study was based on a MASLD population from hospital-based databases across 11 centers nationwide in China, according to MASLD diagnostic criteria identified using keywords and ICD-10 codes. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between risk factors and extrahepatic cancers.

A total of 103,652 individuals with MASLD were identified, among whom 6,605 were diagnosed with extrahepatic cancers. The primary outcome revealed that hypertension was significantly associated with extrahepatic cancers (OR 1.14, 95% CI: 1.08–1.21), and its combination with hyperglycemia further increased this association (OR 1.36, 95% CI: 1.22–1.51). Risk factors for extrahepatic cancers included being over 40 years of age and female sex. Conversely, certain metabolism-based treatments were found to have potentially protective effects, including angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers, fibrates, GLP-1 receptor agonists, and thiazolidinediones. After adjusting for confounding factors, the fibrosis-4 (FIB-4) score was associated with extrahepatic cancers. In the hypertension subgroup, FIB-4 scores of 1.30–2.66, 2.67–3.47, and ≥ 3.48 were associated with extrahepatic cancers in individuals aged 35–64 years, consistent with findings in those aged ≥ 65 years of age with FIB-4 ≥ 2.

Hypertension combined with liver fibrosis is associated with extrahepatic cancers in patients with MASLD.

Pulmonary arterial hypertension (PAH) is a progressive cardiovascular disease with an increasing global burden. Although hemolytic disorders are established causes of PAH, their contribution to the global PAH burden remains unclear. This study aimed to evaluate the association between hemolysis-associated disorders and PAH incidence and to identify the relative contribution of hemolytic disorder subtypes compared with socio-demographic factors.

Using Global Burden of Disease 2021 data, temporal trends in the age-standardized incidence rate (ASIR) of PAH were analyzed using Joinpoint regression. Pearson correlation analysis assessed associations between PAH ASIR and the age-standardized prevalence rates of hemolytic disorder subtypes, hemolysis-related infections, malnutrition, and the Socio-demographic Index (SDI). Random forest regression was used to quantify the contributions of hemolytic disorders to PAH ASIR. Geographic distributions of PAH incidence and hemolytic disorder prevalence were compared, and Bayesian age-period-cohort modeling was used to project their burdens through 2050.

Global PAH ASIR increased from 0.50 to 0.52 per 100,000 from 1990 to 2021. The prevalence of hemoglobinopathies and hemolytic anemias correlated positively with PAH ASIR (R = 0.61, P = 7.70 × 10-22). The random forest model explained 73% of the variance in PAH ASIR (R² = 0.73, P = 0.01), with G6PD trait (percentage increase in mean squared error [%IncMSE]: 18.43), other hemoglobinopathies/hemolytic anemias of unknown etiology (%IncMSE: 18.38), and vitamin A deficiency (%IncMSE: 17.27) identified as the top predictors, surpassing SDI (%IncMSE: 13.25) and sex (%IncMSE: 1.25). Temporal changes in hemolytic disorder prevalence strongly mirrored changes in PAH incidence (R = 0.76, P = 6.34 × 10-39). Exploratory analyses suggested that natural product exposures may contribute to the unexplained hemolytic burden that drives PAH. Projections indicated a continued rise through 2050 in both PAH burden (ASIR increasing from 0.52 in 2022 to 0.57 per 100,000) and hemolytic disease burden (prevalence rising from 27,760.54 to 31,863.72 per 100,000).

Hemolysis-associated disorders, particularly G6PD trait, other hemoglobinopathies/hemolytic anemias, and vitamin A deficiency, are the predominant contributors to the global PAH burden. The projected continued rise in hemolytic disorder prevalence through 2050 signals a persistent exacerbation of the global PAH burden, underscoring the urgent need for targeted prevention strategies.

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.

Mitochondrial DNA (mtDNA) variability, especially heteroplasmy, is believed to affect cellular immunobiogenesis, particularly in monocytes in metabolic syndrome (MetS). This study aimed to identify associations of monocytic mtDNA variability with its phenotypic indices, including cytokine secretion and gene expression, and cardiometabolic parameters in patients with MetS.

The cross-sectional study recruited 87 adult participants, including 34 healthy blood donors (Control group), 21 obese patients (Obesity group), and 32 MetS patients (MetS group). Blood biochemistry tests were performed on venous blood samples, and monocytes (CD14+ cells) were isolated. Monocyte mtDNA was analyzed by next-generation sequencing to identify low (5–10%) and intermediate (10–95%) heteroplasmy, and homoplasmy (≥95%). Expression of genes related to mitochondrial biogenesis, mitochondrial uncoupling, oxidative stress system, and NF-κB signaling was assessed by quantitative real-time polymerase chain reaction. Monocytes cultured with and without lipopolysaccharide for 24 h were analyzed by enzyme-linked immunosorbent assay to assess the cytokine secretion stimulation index.

Monocyte mtDNA showed low variability, but alternative homoplasmies were significantly more common. Intermediate and low heteroplasmy from the protein-coding locus correlated with stenosis (r = 0.396; 95% confidence interval (CI) 0.067–0.647) and low-density lipoprotein levels (r = −0.258; 95% CI −0.45 – −0.043). Intermediate heteroplasmy from the rRNA locus correlated with blood insulin levels (r = −0.228; 95% CI −0.424 – −0.019). D-loop low heteroplasmy correlated with fasting blood glucose (r = 0.275; 95% CI 0.062–0.464). Homoplasmies were associated with creatinine, blood urea nitrogen, and alkaline phosphatase. Intermediate heteroplasmy in mtDNA was associated with the monocyte cytokine secretion stimulation index (R2 = 0.156, P = 0.003). However, there was no significant association between mtDNA variability and the expression of the various genes.

Monocyte mtDNA shows relatively low variability. Low and Intermediate heteroplasmy are associated with cardiometabolic parameters, and intermediate heteroplasmy is associated with the monocyte cytokine secretion stimulation index.