The mortality rate from coronary atherosclerotic heart disease is rising year by year, affecting an increasingly younger population, and is projected to continue rising in the future. Although medical technology is advancing, coronary angiography cannot be widely adopted for screening due to factors such as economic constraints, disparities in regional healthcare standards, and patient compliance. This study aimed to develop and validate a machine learning-based predictive model for assessing the severity of coronary artery lesions and to explore related risk factors.

This retrospective study included 400 patients who underwent their first complete coronary angiography at the First Affiliated Hospital of Hainan Medical University between 2023 and 2025. The patient dataset from July 2023 to July 2025 (n = 300) was randomly divided into an internal training set and a test set in a 7:3 ratio. The temporal validation set consisted of patients (n = 100) from the same center between August and December 2025. Key feature variables were used to construct predictive models using eight machine learning algorithms, including Extreme Gradient Boosting (XGBoost), Logistic Regression (LR), Random Forest (RF), Support Vector Machines (SVM), K-Nearest Neighbors (KNN), Artificial Neural Networks (ANN), Naive Bayes (NB), and Gradient Boosting Machines (GBM). Model performance was analyzed using receiver operating characteristic (ROC) curves, 10-fold cross-validation, and decision curve analysis (DCA). The optimal model was validated on the temporal dataset, and its interpretability was assessed using SHapley additive explanation (SHAP). The model was further successfully implemented as a web application using the Shiny package (version 1.13.0) in R 4.5.2.

Ten predictors were retained. The XGBoost model exhibited the best discrimination, with AUCs of 0.889 (95% CI: 0.819-0.945) in the internal test set and 0.803 (95% CI: 0.718-0.888) in temporal validation. The model also showed good calibration and low Brier scores, with stable performance in ten-fold cross-validation. DeLong's test confirmed its superiority over competing models. DCA and SHAP analysis further supported its clinical utility and interpretability.

This study developed a machine learning model for predicting the severity of coronary lesions, demonstrating satisfactory performance in a single-center setting.

Pulmonary hypertension (PH) is common in patients undergoing transcatheter mitral edge-to-edge repair (M-TEER) and is an established determinant of adverse outcomes after intervention. Importantly, persistent PH after technically successful M-TEER remains associated with ongoing symptoms, right ventricular dysfunction and poor prognosis, yet no dedicated treatment strategy has been established. The aim of this study is to evaluate the safety and efficacy of pulmonary artery denervation (PADN) in patients with persistent PH following successful M-TEER. Six patients (median age 69.0 years; 1 female) with WHO Group 2 PH and persistent symptoms despite successful M-TEER underwent PADN at a median of 583 days after valve repair. All patients had trace to mild residual MR (grade 1+) with median mean mitral valve gradient 3.0 mmHg. Right heart catheterization (RHC) was performed at baseline, immediately post-PADN, and at 6-month follow-up. Immediately post-PADN, mean pulmonary artery pressure (mPAP) decreased from 38.5 (3.8) mmHg to 34.0 (11.5) mmHg (p = 0.028). Pulmonary arterial wedge pressure decreased from 22.5 (7.5) mmHg to 20.0 (6.2) mmHg (p = 0.026). At 6-month follow-up, a directional but statistically non-significant trend toward maintained mPAP reduction was observed [median 32.5 (9.0) mmHg vs. baseline 38.5 (3.8) mmHg; p = 0.075]. Tricuspid regurgitation grade improved in 5 of 6 patients (83%). Median 6-min walk distance increased from 377 (109) m to 436 (109) m (p = 0.046). No procedural complications occurred. PADN appears feasible, safe, and potentially effective in patients with persistent PH following M-TEER, warranting further investigation in controlled studies.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and a growing public health concern. Its core pathological features include cerebral amyloid-β deposition and tau aggregation. mRNA translation is a tightly regulated process essential for gene expression and protein synthesis. It plays critical roles in neural development, synaptogenesis, and synaptic plasticity. In recent years, dysregulated translational control has been recognized as an important pathogenic mechanism in several neurological diseases, including AD. This review provides an integrated overview of the biological basis and mechanisms of dysregulated mRNA translation in AD, including translation initiation and elongation, local synaptic translation, abnormalities in RNA-binding proteins and stress granules, tRNA dysregulation, and the effects of AD-related genetic factors on translational control. Beyond the classic mechanisms of protein aggregation, the onset and progression of AD are also accompanied by abnormal translational regulation, involving initiation, elongation, and local synaptic translation. A major feature of these abnormalities is the coexistence of suppressed global protein synthesis and selectively enhanced translation of certain disease-related mRNAs, involving the integrated stress response, eIF2α/eIF4E signaling, eEF2K/eEF2 pathway, and RNA-binding protein dysfunction. Translational dysregulation provides a new perspective for understanding the molecular pathology of AD and has prompted the exploration of interventions targeting key nodes in translational control. Strategies targeting the integrated stress response, cap-dependent translation initiation, eEF2K, and tau-RNA-binding protein interactions have shown potential to improve synaptic function and cognitive phenotypes in animal models, although their safety and clinical translatability require further evaluation. This review provides an up-to-date reference for understanding translation-centered mechanisms in AD and evaluating emerging therapeutic strategies targeting translational control.

Post-stroke cognitive impairment (PSCI) is a common and debilitating neurological complication following cerebral ischemia-reperfusion injury (CIRI). The traditional neuron-centered view cannot fully explain its delayed onset, pathological heterogeneity, and functional plasticity. This review proposes a novel neuroecosystem framework based on the neurovascular-immune-glial (NIG) triad, including a systematic evaluation of the dynamic crosstalk among the neurovascular unit (NVU), neuronal networks, and glial-immune microenvironment. Pathological events, including ferroptosis, neuroinflammation, white matter damage, and gut-brain axis dysfunction, are reinterpreted as manifestations of neuroecosystem collapse, rather than isolated lesions. We further summarize cutting-edge tools, such as spatial omics and in vivo dynamic imaging for framework validation, and clarify how therapeutic strategies are shifting from single neuronal protection to overall ecosystem restoration. Finally, we discuss current limitations in knowledge and future research directions, aiming to provide new insights for mechanistic exploration and clinical intervention of PSCI.

Spironolactone (SPL) is a steroidal mineralocorticoid receptor antagonist (MRA) that binds non-specifically to sex hormone receptors. Given the role of sex hormones in sleep regulation, SPL may pose a theoretical risk of insomnia through off-target activity. Recently introduced, esaxerenone (ESAX) is a non-steroidal MRA with high mineralocorticoid receptor selectivity, attracting attention for its potentially favorable safety profile.

This study was conducted to compare the risk of insomnia between SPL and ESAX. Individuals with a history of hypertension who newly initiated either agent were enrolled from the DeSC database. Inverse probability of treatment weighting was used to assess differences in insomnia incidence between treatment groups.

We analyzed 5,091 individuals without a history of insomnia: 1,910 received SPL and 3,181 received ESAX. The median age was 72 (interquartile range [IQR], 67-79) years, 55% of participants were male, and the median estimated glomerular filtration rate was 66.3 (IQR, 56.1-76.2) mL/min/1.73 m². Over a median follow-up of 512 (IQR, 240-848) days, 356 insomnia events were observed. Weighted Cox regression analysis indicated a significantly higher risk of incident insomnia among SPL users than ESAX users (hazard ratio [HR], 1.66; 95% confidence interval [CI], 1.32-2.10). In sex-stratified analyses, the HRs were 1.79 (95% CI, 1.30-2.47) for men and 1.59 (95% CI, 1.15-2.20) for women.

Using a nationwide claims database, we demonstrated that, compared with ESAX, SPL use was associated with a greater likelihood of developing insomnia.

Cardiovascular diseases (CVD) are among the leading causes of mortality worldwide and accurate diagnosis is important for treatment and prognosis. The present study intended to develop a model for diagnosing and classifying cardiovascular diseases to improve early diagnosis precision. The present retrospective study analyzed 116 cases of coronary artery disease (CAD), 26 cases of structural heart disease (SHD), and 58 cases of arrhythmias, along with 200 healthy controls. The present study analyzed the differences in demographic characteristics, clinical symptoms, cardiovascular biomarker levels and electrocardiogram results across these four groups. Multivariate logistic regression and random forests were used to identify significant factors in cardiovascular disease. A diagnostic model was constructed based on the selected factors, and its ability to diagnose cardiovascular diseases and differentiate between CAD, SHD and arrhythmias was evaluated. Patients with CVD showed significant differences compared with the healthy control group in demographic characteristics, including age, sex and family history. Different types of patients with CVD showed varying degrees of symptoms such as pain, dyspnea, and dizziness and there are significant differences in the levels of cardiovascular biomarkers. Cardiac Troponin I, creatine kinase MB, myoglobin and N-terminal pro B-type natriuretic peptide were identified as significant predictors of CVD. The diagnostic model for CVD achieved an Area Under the Curve (AUC) of 0.719, outperforming the use of individual biomarkers. The model differentiated arrhythmias from SHD with an AUC of 0.771 and SHD from CAD with an AUC of 0.715. The diagnostic model offers improved predictive ability for early cardiovascular disease diagnosis compared with standard methods and demonstrates clear advantages when distinguishing between CAD, SHD, and arrhythmias, supporting improved clinical decision-making.

The ENABLE study demonstrated comparable survival benefits between enzalutamide (ENZ) and abiraterone plus prednisolone (ABI) in castration-resistant prostate cancer (CRPC). Although the association between androgen receptor signaling inhibition and cardio-cerebrovascular diseases (CCVDs) has long been discussed, definitive evidence remains limited. We evaluated the efficacy of these agents in patients with CRPC who have CCVDs.

This investigator-initiated, multicenter, randomized controlled trial allowed enrollment of patients with prior or concurrent CCVDs. Prespecified end points included time to prostate-specific antigen (PSA) progression (TTPP), radiographic progression-free survival (rPFS), overall survival (OS), prostate cancer-specific survival (PCSS), and safety. Outcomes were compared between patients with and without CCVDs (CCVD- vs CCVD+) and between treatment arms within each group.

The CCVD- group included 142 patients (75 ENZ and 67 ABI), and the CCVD+ group included 36 patients (14 ENZ and 22 ABI). The most frequent CCVD was cerebral infarction (n = 11, 31%). Survival outcomes did not differ significantly between patients in the CCVD- group and those in the CCVD+ group (median TTPP 15.2 vs 21.2; p = 0.8001; rPFS 18.1 vs 9.4; p = 0.0971; OS 37.4 vs 30.5; p = 0.1793; PCSS 46.8 vs 32.1; p = 0.6348). Within both groups, ENZ and ABI showed no significant differences in TTPP, rPFS, OS, or PCSS. Adverse event rates were also comparable across CCVD groups and treatment arms.

Patients with CCVDs showed no significant differences in survival or safety compared with those without CCVDs, and ENZ and ABI produced similar outcomes in both groups. These findings indicate that both agents remain feasible options irrespective of CCVD history.

The trial was registered with the University Hospital Medical Information Network (UMIN) Center under the identifier UMIN000015529 on November 1, 2014.

Platelet-derived growth factor-BB (PDGF-BB), a core functional isoform of the PDGF family, serves as a central regulator of cell proliferation, migration, differentiation, and tissue remodeling. Extensive preclinical and clinical evidence indicates that PDGF-BB expression exhibits profound spatiotemporal heterogeneity during natural aging and across various pathological conditions, including cardiovascular, neurodegenerative, and musculoskeletal diseases, as well as malignancies. Importantly, these dynamic expression patterns are intrinsically linked to disease progression and distinct aging phenotypes. Mechanistically, PDGF-BB initiates complex intracellular signaling cascades-such as the ERK, JNK, PI3K-AKT, and mTOR pathways-via specific engagement with PDGFRα/β dimers. Through these networks, PDGF-BB orchestrates intercellular communication and maintains microenvironmental homeostasis in a highly dose-dependent and cell-type-specific manner. Consequently, pharmacological interventions using small molecules, natural products, and biological agents have demonstrated efficacy in modulating PDGF-BB expression and its downstream signaling, presenting promising therapeutic targets for aging-related disorders and associated tissue damage. This review systematically synthesizes the heterogeneous expression profiles of PDGF-BB across natural aging and diverse disease contexts. We delineate the molecular mechanisms underlying its role in driving senescence and pathological progression, and critically evaluate the translational potential and current limitations of PDGF-BB-targeted therapies. By comprehensively mapping the biological network of PDGF-BB, this review aims to provide a conceptual framework for future basic research and clinical translation.

Current guidelines advise against routine use of parenteral anticoagulation therapy (PACT) for ST-segment elevated myocardial infarction (STEMI) patients after percutaneous coronary intervention (PCI). However, the effectiveness of PACT in such patients with high thrombotic risk remains uncertain. To determine the impact of PACT on STEMI patients with high thrombotic risk.

We enrolled STEMI patients with high thrombotic risk from four Chinese hospitals between 1 January 2010, and 31 December 2022. STEMI patients with high thrombotic risk were categorized them into PACT and non-PACT groups. We used multivariate, propensity score, and subgroup analyses to examine the relationship between PACT and clinical outcomes. The primary outcomes were in-hospital all-cause death and in-hospital major bleeding.

Out of 2,001 PCI patients, 473 received PACT. PACT was not associated with a lower all-cause death (adjusted OR, 0.70; 95% CI, 0.33-1.48; P = 0.349) and was not associated with an increased risk of major bleeding (adjusted OR, 0.84; 95% CI, 0.32-2.18; P = 0.720). After a median follow-up of 1.72 years, PACT did not significantly affect all-cause death and major adverse clinical events compared to non-PACT, as confirmed by propensity score and subgroup analyses.

PACT was not statistically associated with a reduced risk of in-hospital all-cause death and an increased risk of major bleeding in STEMI patients with high thrombotic risk.

To explore the disease-specific performance of diffusion tensor imaging analysis along the perivascular space (DTI-ALPS) index in cerebral amyloid angiopathy (CAA) and arteriolosclerosis CSVD (aCSVD).

We retrospectively enrolled probable CAA or aCSVD patients who underwent 5.0T MRI. Disease-specific DTI-ALPS characteristics and the correlations with clinical, imaging markers, and cognition were evaluated. Regression models were applied according to outcome distributions. Multiple comparisons were controlled using the Benjamini-Hochberg false discovery rate (FDR) procedure.

A total of 134 participants (56 probable CAA and 78 arteriolosclerosis, mean age 64.9 ± 10.0 years, 64.9% males) were enrolled. DTI-ALPS index was significantly lower in aCSVD than in CAA (p < 0.001). After adjustment for age and sex and FDR correction, no clinical factors remained significantly associated with DTI-ALPS index. In aCSVD, DTI-ALPS was significantly associated with cognitive performance, whereas these associations did not reach statistical significance in CAA. Across both groups, DTI-ALPS was significantly associated with white matter hyperintensity volume, skeletonized fractional anisotropy, skeletonized mean diffusivity, and peak width of skeletonized mean diffusivity (all FDR-adjusted p < 0.05). Associations with PVS burden and established CAA imaging markers did not reach statistical significance.

DTI-ALPS index is heterogenous across distinct angiopathies but consistently associated with white matter microstructural damage. These subtype-specific findings question the relevance of DTI-ALPS index and caution against using DTI-ALPS index as a universal glymphatic surrogate.