Heart failure is a significant disease that threatens human life and health globally, yet its pathogenesis remains incompletely understood, posing challenges for targeted treatment. The pleiotropic transcription factor c-Myc participates in the regulation of various biological processes and has been extensively studied in the field of oncology. Recent studies have increasingly indicated that c-Myc is also associated with the development of non-oncological diseases such as heart failure, playing a role in regulating key biological processes including cardiac hypertrophy, cardiac fibrosis, energy metabolism, and cardiac regeneration and repair in heart failure. This article reviews the latest research progress on c-Myc in heart failure, discussing its role in the pathogenesis of heart failure, its clinical significance, its potential as a therapeutic target, and the regulatory effects of traditional Chinese medicine on c-Myc. c-Myc is widely involved in the pathological process of the occurrence and development of HF, but its function is highly diverse. The specific effects of c-Myc vary considerably depending on the pathological context, disease stage, and its expression level. Current research on c-Myc is primarily at the preclinical stage. In order to facilitate the clinical translation of c-Myc as a potential therapeutic target for HF, future research may focus on precise targeting of c-Myc, optimal expression and timing, exploration of its mechanisms, and the potential of traditional Chinese medicine in modulating its effects.

Early infancy represents a critical window of immune system maturation during which transient dysregulation may result in atypical inflammatory or autoimmune-like phenotypes. Distinguishing such self-limited processes from true systemic autoimmune disease remains a major clinical challenge. We report an infant presenting with prominent cutaneous manifestations, markedly elevated inflammatory markers, hypocomplementemia, and broad high-titer autoantibody positivity including antinuclear, anti-dsDNA, extractable nuclear antigen, and antineutrophil cytoplasmic antibodies. Despite a laboratory profile strongly suggestive of systemic autoimmune disease, the patient remained clinically stable without evidence of organ involvement, including renal, neurological, or cardiopulmonary systems. Immunophenotyping demonstrated lymphocytosis with expansion of CD19+ B cells, while T-cell subsets and natural killer cells remained within expected ranges. Interferon signature analysis was negative, and whole-exome sequencing did not identify a causative monogenic disorder. All immunological abnormalities resolved spontaneously without immunosuppressive therapy. During follow-up, the patient developed transient neutropenia and atopic dermatitis, both with a self-limited course. This case highlights a transient systemic immune phenotype characterized by expansion of the CD19+ B-cell compartment, broad humoral immune activation and complement consumption in early infancy, followed by complete restoration of immune homeostasis. Recognition of such self-limited immune dysregulation is essential to avoid unnecessary immunosuppressive therapy and provides insight into mechanisms of immune tolerance during early human development.

Post-percutaneous coronary intervention (PCI) outcomes in acute myocardial infarction (AMI) remain heterogeneous despite guideline-directed therapy and lower low-density lipoprotein cholesterol (LDL-C) targets. We employed unsupervised clustering of cardiometabolic biomarkers to uncover novel clinical phenotypes that conventional stratifications overlook.

K-means clustering was applied to 13 standardized cardiometabolic variables in 668 AMI patients who underwent successful PCI. Cluster stability was assessed by bootstrap resampling. Clinical outcomes were evaluated by Kaplan-Meier analysis and multivariable Cox regression. Receiver operating characteristic curves and DeLong testing compared discriminative performance between phenotype classification and LDL-C target attainment.

Three phenotypes were identified: Ph0 Metabolically Balanced (n = 391, 58.5%), Ph1 Hyperglycemic-Dyslipidemic (n = 107, 16.0%), and Ph2 Decompensated Inflammatory-Catabolic (n = 170, 25.4%). Over a median follow-up of 31.9 months, major adverse cardiovascular and cerebrovascular events (MACCE) occurred in 19.4%, 31.8%, and 49.4%, respectively (P < 0.001). After full covariate adjustment, Ph2 remained independently associated with MACCE (hazard ratio 2.97, 95% confidence interval 2.00-4.41, P < 0.001), while Ph1 was attenuated to non-significance (P = 0.136). Despite having the lowest LDL-C, Ph2 carried the highest event rate. LDL-C target attainment (<1.8 mmol/L) did not discriminate MACCE risk [area under the curve (AUC) 0.503], whereas phenotype classification yielded an AUC of 0.626 (DeLong P < 0.001).

Unsupervised cardiometabolic phenotyping identified a decompensated inflammatory-catabolic phenotype that carried the highest MACCE risk despite having the lowest LDL-C, representing a high-risk subgroup unrecognizable by conventional lipid-centric stratification. These findings suggest that multi-dimensional metabolic profiling may complement LDL-C targets for residual risk identification in post-PCI AMI patients.

Gastrointestinal bleeding after coronary artery bypass grafting (GIBCG) is a serious postoperative complication linked to increased mortality. The stress hyperglycemia ratio (SHR) has been recognized as a reliable predictor of adverse clinical outcomes, particularly in patients with cardiovascular disease. This study aimed to investigate the association between SHR and both GIBCG and in-hospital mortality.

Patients were recruited from four medical centers and the Medical Information Mart for Intensive Care IV, with a total of 16,440 individuals included in the final analysis. Patients were categorized into four groups based on SHR quartiles. The primary outcomes of interest were the incidence of GIBCG and in-hospital mortality. Restricted cubic splines and logistic regression models were employed to analyze the relationship between SHR and clinical outcomes.

Among the patients who underwent surgery, 1,158 (7.04%) experienced GIBCG, while 214 (1.3%) died during hospitalization. After adjusting for confounding variables, a U-shaped relationship was observed between SHR and both GIBCG occurrence and in-hospital mortality. The lowest incidence of these outcomes was observed within the SHR range of 0.706-0.792, with inflection points identified at 0.71 for GIBCG and 0.733 for in-hospital mortality.

A U-shaped relationship was identified between SHR and both GIBCG and in-hospital mortality. Both low and high SHR levels may help identify patients at increased risk of gastrointestinal bleeding and in-hospital mortality following coronary artery bypass grafting.

To construct a dual-energy computed tomography (DECT) parameter-radiomics combined model based on DECT quantitative parameters and radiomic features and to evaluate its diagnostic performance in differentiating benign from malignant solitary pulmonary nodules.

We retrospectively collected data from inpatients who underwent contrast-enhanced thoracic DECT scans at our hospital between June 2018 and November 2024. Quantitative parameters measured and calculated included iodine concentration, effective atomic number, normalized iodine concentration, normalized effective atomic number, spectral Hounsfield unit slope, and extracellular volume fraction. These DECT parameters were used to construct a predictive model. The dataset was randomly divided into training and test sets in a 7:3 ratio. Radiomic features were extracted from mixed-energy images of the arterial and venous phases (A_120kVp and V_120kVp) and from 70-keV monoenergetic images (A_70keV and V_70keV). Six machine-learning algorithms were used to construct radiomics models, and the optimal model was selected based on performance. This optimal radiomics model was then combined with the DECT parameter model to create the combined model. Model performance was evaluated using accuracy, sensitivity, specificity, and area under the curve (AUC), and model comparisons were performed using the DeLong test (Python). A P-value of<0.05 was considered statistically significant.

In total, 209 patients were enrolled (166 in the malignant group and 43 in the benign group). In the test set, the diagnostic performance of the combined model (AUC = 0.906) exceeded that of the DECT-only radiomics model (AUC = 0.794). The combined model demonstrated an accuracy of 82.5%, sensitivity of 80.0%, and specificity of 92.3%.

The DECT parameter-radiomics combined model effectively differentiated benign from malignant solitary pulmonary nodules and shows promising potential for clinical translation.

Intracranial atherosclerotic disease (ICAD) is one of the important causes of ischemic stroke worldwide. With advances in patient selection, perioperative management, and endovascular device technology, endovascular therapy (EVT) has become an important research focus in ICAD as a potential adjunctive treatment strategy. This review summarizes the current global status of ICAD management, with particular attention to regional differences in epidemiological characteristics, endovascular treatment strategies, and perioperative medical management. This review may help improve understanding of the evolving treatment strategies and regional differences in ICAD management and provide references for future precision-based and individualized neurointerventional therapy.

Atherosclerosis (AS), which causes chronic inflammation, aberrant lipid metabolism and vascular endothelial damage, is the main cause of cardiovascular disease. The Ce-Bai-Si-Wei decoction (CSD) may reduce AS, although its molecular mechanisms are unknown. This study investigates core molecular pathways using multi-omics integration and experimental validation.

Network pharmacology prediction: Construct a 'drug-component-target-disease' interaction network using databases like TCMSP, HIT and ETCM to identify active components and targets of CSD. AS regulatory targets and signalling pathways can be identified by integrating microarray data and single-cell transcriptomics data. In vitro validation: Utilise the OX-LDL-induced model of macrophage foam cells to test CSD's effects on lipid accumulation utilising CCK-8, Oil Red O and TC/TG quantification. Validate CSD's regulatory effects on core targets using molecular docking, molecular dynamics simulation, RT-qPCR and Western blot.

Four core genes, HMOX1, SELE, CD4 and FLT1, were identified as key regulators of inflammation and oxidative stress in AS, and they bind stably to the active components of CSD. Single-cell data analysis suggested that CSD may improve AS by targeting macrophages and endothelial cells. In vitro, CSD reduced ox-LDL-induced lipid accumulation in macrophages and downregulated TNF-α and IL-1β. Mechanistically, the anti-AS effect of CSD depends on the NRF2/HMOX1 pathway. CSD also downregulated FLT1 and SELE in damaged endothelial cells.

This study investigated the mechanism of CSD in treating AS. CSD acts on the core targets HMOX1, SELE, FLT1 and CD4, with macrophages and endothelial cells as key effector cells. It exerts anti-AS effects by inhibiting inflammation, reducing lipid accumulation and protecting endothelial function.

Extracellular vesicles (EVs) are nanoscale membrane-bound structures that play a pivotal role in intercellular communication by transporting bioactive molecules, including proteins, lipids, nucleic acids, and organelles, between cells. Originating from the endosomal pathway, EVs reflect the physiological and pathological status of their parent cells and participate in a broad range of biological processes, such as immune regulation, tissue regeneration, and disease progression. This review provides a comprehensive overview of EVs' biology, covering their biogenesis, biochemical composition, isolation strategies, and characterization methodologies. Recent advances in quantitative, qualitative, and single-vesicle analytical techniques are discussed, highlighting both their advantages and technical limitations. Emphasis is placed on the functional roles of EVs in cancer, cardiovascular diseases, autoimmune disorders, intestinal fibrosis, and neural repair, with a focus on their contributions to disease pathogenesis, biomarker discovery, and therapeutic resistance. Furthermore, emerging strategies employing both natural and engineered EVs as therapeutic delivery platforms are examined. Special attention is given to EVs-integrated hydrogel systems designed to improve bioavailability, enhance retention at target sites, and enable controlled therapeutic release. Despite their considerable therapeutic potential, several challenges remain, including the need for standardized isolation protocols, scalable production, management of vesicle heterogeneity, and successful clinical translation. Overall, this review highlights the multifaceted biological significance of EVs and underscores their increasing potential as diagnostic biomarkers and next-generation therapeutic platforms across a wide range of disease conditions.

Accurate identification of anatomical structures is essential for safe congenital cardiac surgery and for the development of assistive robotic systems. However, scalable annotation of open-heart surgical video remains a major challenge due to dynamic tissue motion, occlusion, and anatomical variability. The aim of this study was to develop and evaluate a human-in-the-loop segmentation and tracking pipeline for congenital open-heart surgery videos. A dataset of 72 annotated video clips comprising 27,461 frames was created from routine recordings of congenital cardiac surgery. Independent tracking evaluation was performed on 6 video clips (2,400 frames) from three surgical cases that were not used for training or validation. A hybrid framework combining fine-tuned Segment Anything Model 2 (SAM 2) for propagation-based tracking and YOLOv11 for detection-based monitoring was implemented and evaluated. Fine-tuning improved temporal tracking performance compared with the pretrained model, increasing the mean IoU from 82.1% to 92.2% and the proportion of frames with IoU ≥ 90% from 48.2% to 72.3% on the independent evaluation dataset. A graphical user interface enabled efficient dataset creation, reducing annotation time by approximately 40-fold compared with manual tracing. This study demonstrates that domain-adapted foundation-model tracking can provide robust anatomical tracking in a dynamic open surgical environment and offers a scalable framework for future assistive and robotic cardiac applications.

Spontaneous angiographic obliteration of brain arteriovenous malformations (SpOAVM) is rare, and published incidence estimates are limited by heterogeneous denominators and variable imaging follow-up. We performed a meta-analysis to estimate the incidence of SpOAVM and to describe associated angioarchitectural features. Literature from 1974 to January 2026 was systematically reviewed in accordance with PRISMA. Observational studies reporting complete spontaneous angiographic obliteration of intracranial arteriovenous malformations (AVMs), without prior AVM-directed therapy, were included. The meta-analysis used a linear mixed model with a rare-event-appropriate log-log link. Denominator definition, imaging modality, follow-up duration, reappearance after apparent obliteration, and angioarchitectural variables were extracted. Nine studies contributed 47 eligible SpOAVMs across 7,922 brain AVMs, although some denominators were mixed or estimated. In four cohorts with definitive no-intervention denominators, pooled SpOAVM incidence was 1.93% (95% confidence interval [CI], 1.04-3.44), corresponding to 0.39 per 100 person-years. Across all eligible studies, including cohorts with uncertain denominator purity, the pooled estimate was 1.08% (95% CI, 0.58-3.05). SpOAVMs most commonly followed hemorrhage (37/45, 82%). Exploratory external-cohort comparisons showed that SpOAVMs had a higher proportion of smaller nidus size and single venous drainage. Reappearance after apparent obliteration was reported in 2/35 cases. SpOAVM is rare and occurs far less frequently than hemorrhage during untreated follow-up. Apparent obliteration requires cautious interpretation because imaging modality and follow-up were heterogeneous. Standardized prospective angiographic surveillance is needed to define clinically relevant subgroups.