Objective: This exploratory study aimed to develop a preliminary nomogram for risk assessment of poor prognosis in spontaneous cervical artery dissection (sCAD) and evaluate its statistical performance using internal validation.
Methods: We retrospectively analyzed 75 patients with sCAD (mean age 51.8 ± 14.0 years; 41 males [55%] and 34 females [45%]) diagnosed between November 2013 and April 2024. Poor prognosis was defined as imaging-confirmed acute cerebral infarction or hemorrhage (n=38); the remaining 37 patients comprised the good prognosis group. Due to the small sample size, variables with p<0.2 in univariate analysis (sex, extracranial CAD type, hypertension, hyperhomocysteinemia) were considered for multivariate modeling, though none were statistically significant predictors (all p>0.05). A multivariate logistic regression-based nomogram was constructed and internally validated using 1000 bootstrap resamples.
Results: The final model included the four variables above. Only non-intramural hematoma (other) CAD type showed statistical significance in the multivariate model (OR=13.41, 95% CI: 2.89-62.17, P<0.01), while sex, hypertension, and hyperhomocysteinemia did not, likely reflecting statistical instability from inadequate power. In bootstrap internal validation, the model demonstrated moderate discrimination (AUC=0.788, 95% CI: 0.686-0.891) with a Brier score of 0.185. Hosmer-Lemeshow test indicated acceptable calibration (χ2=8.11, P=0.23). Mean AUC across bootstrap samples was 0.763 (95% CI: 0.662-0.863), suggesting minimal overfitting within this dataset, though this does not imply generalizability.
Conclusion: This pilot study generates the hypothesis that ultrasonographic CAD type, combined with clinical variables, may aid in predicting sCAD outcomes. However, due to the small sample size (9.5 events/variable), lack of external validation, and inclusion of non-significant predictors, this model is not ready for clinical application. Multi-center prospective validation in a cohort of at least 400 patients is required before any clinical utility can be claimed.
Objective: To investigate whether fragmented QRS (fQRS) on electrocardiogram (ECG) obtained 24-48 hours after percutaneous coronary intervention (PCI) predicts left ventricular remodeling (LVRM) and major adverse cardiovascular events (MACE) in patients with acute myocardial infarction (AMI).
Methods: A total of 122 AMI patients who underwent PCI were prospectively enrolled and categorized into fQRS (n=48) and non-fQRS (n=74) groups based on post-PCI ECG findings. Clinical data, serum biomarkers, left ventricular function, and the incidence of MACE were compared between groups. Cox proportional hazards regression and logistic regression analyses were used to identify independent predictors of MACE and LVRM, respectively.
Results: Patients in the fQRS group exhibited significantly higher levels of cardiac biomarkers (cTnI, CPK, CK-MB), more adverse lipid profiles, and impaired renal function parameters (all P < 0.05). Echocardiographic assessment revealed significantly reduced left ventricular ejection fraction (51.5% vs 57.2%, P < 0.001) and increased wall thickness in the fQRS group. During one-year follow-up, the fQRS group had a substantially higher incidence of MACE (35.4% vs 10.8%, P < 0.001). Multivariate analysis confirmed post-PCI fQRS as an independent predictor for both LVRM (OR: 3.12, 95% CI: 1.48-6.55, P = 0.003) and MACE (HR: 2.65, 95% CI: 1.52-4.63, P = 0.001).
Conclusion: fQRS identified on ECG after PCI is a significant independent predictor of LVRM and MACE in AMI patients, providing valuable prognostic information for risk stratification.
Objective: To investigate the impact of Rho GTPase-activating protein 33 (ARHGAP33) and its synergistic interaction with SFPQ on the prognosis of hepatocellular carcinoma (HCC) through bioinformatics and experimental research.
Materials and methods: RNA sequencing data from The Cancer Genome Atlas (TCGA) were analyzed to assess ARHGAP33 expression in hepatocellular carcinoma (HCC). Co-expressed genes were identified using WGCNA and GSVA, and integrated into a multi-algorithm consensus prognostic model.
Results: The analysis of the TCGA database indicated a marked overexpression of ARHGAP33 mRNA in tissues from hepatocellular carcinoma (LIHC), with a statistically significant finding (P < 0.001). WGCNA revealed that SFPQ is a gene associated with ARHGAP33. In the developed consensus prognostic model, survival analysis using Kaplan-Meier (K-M) alongside the CoxBoost model demonstrated that the overall survival time for patients classified as high-risk was significantly less than that of those classified as low-risk (P < 0.05).The Institutional Review Board at Shihezi University granted ethical approval for this research (Ethics Application No.: KJ2025-290-01).
Conclusion: The expression level of ARHGAP33 affects HCC prognosis, and its synergistic overexpression with SFPQ impairs the prognosis of HCC patients. ARHGAP33 could potentially be used as a biomarker for evaluating prognosis in hepatocellular carcinoma (HCC), offering a new theoretical foundation for enhancing HCC outcomes.
Objective: This study aims to investigate the mechanism of AGS-IV in treating diabetic cardiomyopathy (DCM) by establishing animal and cellular models of the disease.
Methods: A DCM rat model was established by feeding a high-fat diet combined with streptozotocin (STZ) injection, and a DCM cell model was created through glucose induction. In model rats, the cardiac weight-to-body weight ratio, the left ventricular weight-to-heart weight ratio, and ventricular wall thickness were measured. ELISA was used to detect Collagen1 and MMP-2 levels in myocardial tissue, serum, and cultured cells. The mRNA levels of GNG2, MRAS, and ERK in myocardial tissue and cultured cells were measured using RT-PCR.
Results: In vivo, experiments demonstrated that AGS-IV effectively reduced the cardiac weight-to-body weight ratio, left ventricular weight-to-heart weight ratio, and ventricular wall thickness in DCM rat models. It also decreased Collagen I levels in myocardial tissue and MMP-2 levels in serum, accompanied by downregulated mRNA expression of GNG2, MRAS, and ERK in myocardial tissue. In vitro, AGS-IV significantly reduced Collagen I and MMP-2 levels in DCM cell models and downregulated GNG2, MRAS, and ERK mRNA expression.
Conclusion: AGS-IV exerts therapeutic effects on DCM by regulating the GNG2/MRAS-ERK signaling pathway.
Spinal cord injury (SCI) is a severe neurotraumatic condition for which effective therapeutic options remain limited, and advances in clinical pharmacological research have been slow. The diverse pathophysiological alterations that occur after SCI initiate cellular pyroptosis, which in turn exacerbates tissue damage, impedes neuronal functional recovery, and connects multiple pathological processes involved in SCI. In recent years, research on natural bioactive compounds has made substantial progress in the field of neurotrauma, including SCI, leading to the identification of several compounds capable of effectively modulating pyroptosis and promoting functional recovery. Therefore, a comprehensive synthesis of the mechanisms underlying pyroptosis during SCI pathophysiology, along with an overview of natural bioactive constituents with the potential to modulate SCI-related pyroptosis, may provide useful insights for future pharmacological studies, mechanistic investigations, and clinical management of SCI.
Purpose: To determine the serum expression profile of miR-377-3p in carotid artery stenosis (CAS) patients and to assess its diagnostic potential in a clinical setting.
Patients and methods: Using qRT-PCR, miR-377-3p expression was measured in serum samples from 78 CAS patients and 78 matched healthy controls. We used the Pearson correlation to analyze inter-indicator relationships and the ROC curve to assess the diagnostic significance of miR-377-3p. The cellular functions of human aortic smooth muscle cells (HASMCs) were assessed. Bioinformatics predictions of target associations were experimentally verified with a luciferase activity assay.
Results: Patients diagnosed with CAS had a lower serum level of miR-377-3p. ROC curve-based analysis showed that miR-377-3p exerted high diagnostic value, where the area under the curve (AUC) was 0.9597. Serum miR-377-3p was negatively correlated with systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG), and low-density lipoprotein cholesterol (LDL), while positively correlated with high-density lipoprotein cholesterol (HDL). miR-377-3p inhibited the proliferation and migration of HASMCs, but this effect was counteracted by EDIL3.
Conclusion: These results suggest the dual utility of miR-377-3p as a promising biomarker and a potential therapeutic target in the management of CAS. miR-377-3p can inhibit the proliferation and migration of HASMCs by targeting EDIL3.
Background: Despite advances in surgical techniques, recurrence after chronic subdural hematoma (CSDH) evacuation remains common. With the aging of the population, the incidence rate is still rising. Most patients require surgical treatment, but postoperative hematoma recurrence remains an important factor affecting patient prognosis.
Objective: This study aimed to identify factors influencing recurrence following neuroendoscopic-assisted drainage.
Methods: CSDH patients who underwent neuroendoscopy-assisted hematoma drainage(NEAHD) via a single burr-hole craniostomy between January 2021 and August 2024 were categorized based on the presence or absence of postoperative hematoma recurrence. Binary logistic regression analysis was performed on the variables that showed statistically significant inter-group differences in univariate analyses.
Results: In total, 121 patients with CSDH were included. The recurrence group consisted of 17 patients (14.05%). Gender, age, smoking, alcoholism, hypertension or diabetes, perioperative use of statins, hematoma thickness, midline deviation distance, and direction, depth, and retention time of the drainage tube were not associated with hematoma recurrence. In contrast, hematoma capsule spanning the Sylvian fissure (P < 0.001; OR = 12.504; 95% CI, 3.091-50.583) and non-blocking the main trunk or major branches of the middle meningeal artery (MMA) (P = 0.006; OR = 9.955; 95% CI, 1.911-51.848) were the independent risk factors for hematoma recurrence after NEAHD surgery.
Conclusion: Spanning of the hematoma capsule over the Sylvian fissure and absence of intraoperative occlusion of the middle meningeal artery are independent risk factors for recurrence. These features should be considered when planning surgical strategies for CSDH.
Purpose: Previous studies have highlighted diverse roles for EGFL7 in various cancers, but its specific function in cervical cancer remains unclear. This study aimed to elucidate the role of EGFL7 in cervical cancer susceptibility and pathogenesis.
Methods: We genotyped three EGFL7 SNPs in 694 healthy controls, 408 cervical intraepithelial neoplasia (CIN) patients, and 934 cervical cancer (CC) patients using TaqMan probe-based real-time PCR. EGFL7 expression was measured in tumor tissues and cell lines via qRT-PCR. RNA sequencing was used to explore the biological functions of EGFL7 in cervical cancer.
Results: The G allele frequency of rs9411260 was significantly elevated in both the cervical cancer (CC) (P = 0.006) and cervical intraepithelial neoplasia (CIN) (P = 0.016) groups compared to the control group. EGFL7 mRNA expression was markedly downregulated in cervical cancer tissues and HeLa/C33A cells compared to normal tissues and ECT1/E6E7 cells. Furthermore, modulation of EGFL7 expression was found to alter pathways associated with cell adhesion, migration, and ECM-receptor interaction.
Conclusion: EGFL7 polymorphisms and expression are associated with cervical cancer susceptibility. Dysregulated EGFL7 appears to contribute to cervical cancer progression by affecting cell adhesion and migration, offering new insights into its pathogenesis and potential therapeutic targets.
Purpose: This study sought to investigate the predictive factors for atrial fibrillation late recurrence (AFLR) and major adverse cardiovascular events (MACEs) in atrial fibrillation (AF) patients after radiofrequency catheter ablation (RFCA) and construct a nomogram prediction model for providing precious information of screening the high risk patients and giving appropriate preventive interventions.
Patients and methods: A total of 128 patients with atrial fibrillation (AF) who underwent RFCA were enrolled. Univariate and multivariate Cox regression were used to screen the predictors of AFLR and MACEs (including rehospitalization due to AF recurrence, heart failure, myocardial infarction, coronary revascularization, stroke and all-cause mortality). The nomogram model was constructed to predict AFLR after RFCA. Risk stratification based on the nomogram further predicted AFLR and MACEs after RFCA. Subgroup analysis and survival analysis of high and low risk groups in individuals with AF after RFCA were performed.
Results: During median follow-up of 76.50 (5.75) months, 71 (55.47%) patients experienced AFLR, while 56 (43.75%) suffered from MACEs. Early recurrence, maximum left atrial volume index (LAVImax) and E/Vp were the independent risk factors for predicting AFLR after RFCA. And AFLR was the only independent predictor for MACEs. Accordingly, a nomogram prediction model based on early recurrence, LAVImax and E/Vp was constructed, the 1-year, 3-year and 5-year AUC of AFLR were 0.904, 0.826 and 0.793, respectively. Risk stratification based on the nomogram had high predictive value for AFLR and MACEs. The Kaplan-Meier survival curves showed great discrimination between the low and high risk groups in the probability of free from AFLR and MACEs.
Conclusion: The nomogram model based on early recurrence, LAVImax and E/Vp can be used to predict the AFLR and MACEs after RFCA accurately and individually, in order to provide scientific and effective patient management basis for AF patients after RFCA.
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