Manual evaluation of non-contrast CT scans (NCTS) for detecting subdural hematoma (SDH) is time consuming, potentially inaccurate, and subjective to the expert analyzing them. In recent years, two deep learning (DL) algorithms have been popularly studied in this respect, namely convolutional neural networks (CNN) and U-Net architectures, the latter being a specialized type of CNN. We performed the first meta-analysis comparing various DL models for SDH detection. MEDLINE, Cochrane, Scopus, and Embase databases were searched from inception through December 2025. Studies evaluating ML model performance on an independent test dataset were included. The main outcome measures were sensitivity, specificity, diagnostic odds ratio (DOR), accuracy, and precision of CNN, U-Net, and hybrid DL models. Univariate meta-regression analyses were performed. 30 testing datasets incorporating 67,266 NCTS were included. U-Net demonstrated significantly higher sensitivity (0.916;p = 0.04) and precision (0.983;p = 0.001) while high specificity, DOR, and accuracy values were consistently observed across all DL techniques. Internal testing (p = 0.05) was a borderline significant predictor of high specificity while recent publication year (p < 0.001), U-Net architecture (p = 0.035), and 3D models (p = 0.022) emerged as significant moderators of high precision. The U-Net architecture was also a borderline significant predictor of high DOR (p = 0.049). While this single arm meta-analysis depicts potential superiority of U-Net models with respect to sensitivity and precision, these findings are based off only 4 pooled U-Net datasets in comparison to the 22 pooled for CNN architectures. Future well-powered studies evaluating the U-Net model are necessary to ensure a fair comparison of U-Net architectures to other DL designs before reaching to any definitive conclusions in this respect.

These guidelines (GLs) aim to improve and standardize the management of post-surgical hypoparathyroidism (hypoPTH) and to ensure that all patients receive the best possible care nationwide.

Adults with post-surgical hypoPTH.

The GLs do not address individuals under 18 years of age or those with familial, genetic, or autoimmune forms of hypoPTH. Patients with advanced renal failure are also excluded.

Direct costs and resource utilization were evaluated over time to implement appropriate management within the National Health Service. Recommendations were formulated based on an analysis of literature evidence according to the GRADE methodology. Patient preferences were collected and verified through targeted bibliographic research and the active participation of two patients within the GLs' development group.

The present GLs provide four formal graded recommendations and 34 ungraded good clinical practice indications. A high level of agreement was consistently achieved among panel members.

These GLs provide operational recommendations-based on the best available evidence -for the treatment of adult patients with post-surgical hypoPTH. The expected benefits of disseminating and implementing these GLs include improved quality of care, national standardization, and the rationalization of healthcare expenditure, while respecting patient preferences.

We integrate evidences from human and mouse model studies which emphasize sphingolipid metabolism-mediated endothelium-lipoprotein-atherogenic plaque framework. The review may provide a new angel for understanding the development of atherosclerosis and its prevention and treatment.

Sphingolipids, such as ceramide, sphingomyelin, glucosylceramide, sphingosine-1-phosphate, are one of the major players in atherogenesis. Atherosclerosis begins when ApoB-containing lipoproteins accumulate and undergo modification in the subendothelial space and then progresses through endothelial dysfunction, leukocyte recruitment, foam-cell formation, and plaque formation. Sphingolipids participate in each of these stages both as structural membrane components and as signaling molecules. In this review, we highlight recent advances in sphingolipid biomarkers and discuss their clinical promise and limitations.

Infective endocarditis (IE) following transcatheter valvular interventions, including transcatheter aortic valve implantation and transcatheter edge-to-edge repair, is an uncommon but life-threatening complication associated with major diagnostic and therapeutic challenges. As indications for structural interventions continue to expand, the burden of device-related IE is expected to increase. This expert opinion, jointly developed by the Association of Valvular Heart Disease and the Association of Cardiovascular Intervention of the Polish Cardiac Society, summarizes contemporary evidence regarding the epidemiology, clinical presentation, diagnosis, treatment, and prevention of transcatheter valve-related IE. Transcatheter aortic valve implantation-related IE occurs at an estimated incidence of 0.3-2.0 per 100 person-years and is associated with high in-hospital and long-term mortality, whereas transcatheter edge-to-edge repair-related IE is less frequent but similarly associated with poor outcomes. Clinical presentation is frequently atypical, particularly in elderly and in patients with multimorbidity, resulting in delayed diagnosis. Echocardiography remains the first-line imaging modality but is often limited by prosthesis-related artifacts. Multimodality imaging, particularly electrocardiography-gated cardiac computed tomography and in selected cases positron emission tomography, substantially improves diagnostic accuracy and detection, especially of perivalvular complications. Management relies on prolonged pathogen-directed intravenous antibiotic therapy, but surgical intervention should be considered in all patients, with a significant indication for surgery in patients with uncontrolled infection, heart failure, embolic complications, or extensive tissue destruction. Preventive measures, including maintaining strict periprocedural asepsis and targeted antibiotic prophylaxis, remain essential. IE after transcatheter valvular interventions therefore represents a rare but devastating complication requiring high clinical vigilance, multidisciplinary management, and individualized treatment strategies to improve outcomes.

Long-term mortality remains unsatisfactorily high after transcatheter aortic valve replacement (TAVR). Conventional risk models are limited in capturing subclinical electrophysiological alterations associated with poor prognosis, which can be identified on routine preoperative electrocardiograms.

The authors aim to develop and validate an artificial intelligence-enhanced electrocardiogram (AI-ECG) model for predicting long-term mortality in post-TAVR patients.

A total of 711 patients with severe aortic stenosis undergoing TAVR were enrolled from 2 centers. Patients from one center were divided into training and internal validation sets (7:3), and participants from another center served as the external validation cohort. Preoperative electrocardiogram images were analyzed using a Residual Network-18 model to generate mortality risk stratification. The primary endpoint was 3-year all-cause death.

The AI-ECG model demonstrated comparable discrimination between the internal and external patient cohorts, with areas under the receiver operating characteristics curve of 0.767 (95% CI: 0.657-0.877) vs 0.712 (95% CI: 0.627-0.795) (P for DeLong test = 0.428). High-risk patients (15.5% [39 of 251]) exhibited a 61.5% (24 of 39, 95% CI: 42.8%-74.1%) 3-year mortality rate vs 16.5% (35 of 212, 95% CI: 11.4%-21.4%) in low-risk patients (84.5% [212 of 251]) (log-rank P < 0.001). Adjusted for comorbidities, high-risk classification independently predicted mortality (adjusted HR: 3.49; 95% CI: 1.96-6.22). Subgroup analysis did not reveal significant interaction effects of the AI-ECG model across different patient populations. Decision curve analysis confirmed clinical net benefit across threshold probabilities (0.05-0.60).

The AI-ECG model provides noninvasive and accurate long-term risk stratification for TAVR patients, with promising clinical application value for individualized follow-up management.

Doxorubicin (DOX) is a potent chemotherapeutic agent whose antitumor benefits are limited by a well-recognized, dose-dependent cardiotoxicity. While previous studies have implicated inflammatory pathways in DOX-induced cardiomyopathy (DIC), the role of CCR2 in this process remains incompletely defined. This study aims to investigate whether CCR2 deficiency confers cardioprotection against DIC and to uncover the molecular mechanisms involved.

CCR2 knockout (CCR2^⁻/⁻ ) mouse was subjected to both acute and chronic DIC models. Bone marrow transplantation was used to establish the functional contribution of CCR2-deficient macrophages. Autophagic flux was evaluated using complementary approaches, including a tandem mRFP-GFP-LC3 reporter, western blotting, immunofluorescence, and transmission electron microscopy. The mediator linking CCR2-deficient macrophages to cardiomyocytes was identified by proteomics and validated using recombinant IL12B protein and a neutralizing antibody.

CCR2 deficiency substantially improved cardiac function, as evidenced by preserved left ventricular ejection fraction, fractional shortening and reduced serum cardiac injury markers. Mechanistic studies revealed that CCR2^⁻/⁻ hearts exhibited enhanced autophagic flux, with increased LC3B lipidation, autophagosome formation, and clearance of damaged cellular components. Proteomic profiling of cardiac macrophages identified interleukin-12B (IL12B) significantly upregulated in CCR2^⁻/⁻ mouse. Recombinant IL12B protein administration activated cardiomyocyte autophagy through PI3K/Akt/mTOR pathway inhibition and reproduced the cardioprotective effects in WT mouse. Conversely, IL12B neutralization completely abolished CCR2 deficiency-mediated protection.

Our findings identify a novel CCR2-IL12B-autophagy axis that critically regulates DOX-induced cardiotoxicity. CCR2 deficiency promotes IL12B secretion from cardiac macrophages, which directly activates protective autophagy in cardiomyocytes. These results establish CCR2 inhibition and IL12B supplementation as two promising therapeutic strategies to prevent chemotherapy-induced cardiomyopathy, providing a transformative approach to cardio-oncology.

Urban tree canopy is known to mitigate ambient heat and improve physical and mental health but the longitudinal interactions and impacts of tree canopy, temperature, and mortality are not well understood. Using high resolution tree canopy estimates, temperature, mortality, and demographic data from 2011 to 2021, we implemented negative binomial generalized estimating equations to model all-cause and disease-specific mortality based on tree canopy cover, year-to-year changes in tree canopy cover, and maximum temperature, adjusting for area-level demographics in Chicago, IL. We used K-means clustering to identify patterns of canopy, temperature, and mortality disparities across Chicago community areas. There were 220,711 decedents during the study period (115,974 male, 104,734 female; mean age at death: 69.4 ± 19.9 years). Existing canopy coverage was not statistically significantly associated with mortality (incidence rate ratio [IRR] = 0.995, 95% confidence interval [CI] = 0.984-1.007). However, each year-to-year percent increase in canopy was associated with around a 10% reduction in mortality (IRR = 0.902, [0.871-0.935]) with significant associations for cause-specific cardiovascular (IRR = 0.908, [0.869-0.948]), mental health (IRR = 0.836, [0.784-0.892]), musculoskeletal (IRR = 0.907, [0.832-0.989]), and respiratory (IRR = 0.887, [0.833-0.945]) diseases. Cluster analysis identified that neighborhoods on Chicago's South and West sides were characterized by high temperatures, greater absolute canopy loss despite elevated baseline canopy levels, and increased mortality. Among the hottest neighborhoods, canopy-temperature interaction models demonstrated that areas experiencing larger year-to-year canopy losses had higher yearly mortality. Protecting tree canopy cover from losses over time, particularly in vulnerable areas with higher temperatures, may present a key opportunity to reduce mortality and mitigate impacts of climate change.

Acute kidney injury (AKI) is a life-threatening clinical syndrome characterized by high mortality, in which tubular epithelial cell death represents a key pathological event. Emerging evidence underscores the importance of the ubiquitin system in the progression of AKI. Here, we focus on the function of YOD1 in AKI.

We generated tubular epithelial cells (TECs)-specific Yod1 knockout mice (YOD1CKO) by crossing Yod1^fl/fl mice and Ggt1-cre mice. Both YOD1CKO mice and Yod1^fl/fl littermates were subjected to cisplatin- or ischemia/reperfusion (I/R)-induced AKI models. Through co-immunoprecipitation (Co-IP) combined with LC-MS/MS analysis, we identified potential substrate proteins of YOD1.

We observed that YOD1 is predominantly expressed in TECs and is upregulated during AKI injury. Renal tubular specific Yod1 knockout significantly alleviated tubular damage and apoptosis in AKI mice. Mechanistically, we identified the pro-apoptotic protein Bax as a direct substrate of YOD1. YOD1 removes K63-linked ubiquitin chains from Bax at lysine 128 via its catalytic cysteine residue C155, thereby promoting Bax activation, and mitochondrial translocation and subsequent apoptosis. YOD1 failed to promote apoptosis in Bax-deficient cells, confirming Bax as the essential downstream mediator.

Our study reveals a previously unrecognized YOD1-Bax regulatory axis that drives tubular apoptosis in AKI, and highlights YOD1 may hold therapeutic potential.

Patients with hypertension are recommended to decrease their salt intake. However, some patients do not follow this recommendation. It is possible that some of these individuals cannot restrict their salt intake due to a genetic preference for salt. Thus, we attempted to identify genetic factors related to salt restriction behavior. The subjects were 817 patients with hypertension. Salt restriction status was determined by self-reported answers (yes/no) to the question "Do you restrict your salt intake in everyday meals?" We focused on 21 single-nucleotide polymorphisms related to genes involved in the regulation of blood pressure, salt metabolism, or neurotransmission, and analyzed the associations of the single-nucleotide polymorphisms with salt restriction behavior. Of the 817 subjects, 568 (69.5%) reported that they restricted their salt intake. Two single-nucleotide polymorphisms (rs1167998 and rs2970847) were found to be correlated with salt restriction behavior. Among the 21 single-nucleotide polymorphisms, rs1167998 in the intron region of the dedicator of cytokinesis 7 gene, which encodes a guanine nucleotide exchange factor that plays a role in axon formation and neuronal polarization, showed the strongest association (odds ratio per allele, 1.48; 95% confidence interval, 1.11 to 1.95). In conclusion, rs1167998, a single-nucleotide polymorphism in the dedicator of cytokinesis 7 gene that is associated with blood lipid levels and cardiovascular disease risk was associated with salt restriction behavior in a population of Japanese patients with hypertension. Further confirmatory studies are warranted.

Pulmonary arterial hypertension associated with congenital heart disease (PAH-CHD) is a cardiopulmonary disorder characterized by pathological pulmonary vascular remodeling and perivascular inflammatory cell infiltration. ADAMTS4 is a secreted, zinc-dependent metalloprotease critically involved in extracellular matrix degradation and turnover and has recently emerged as a potential biomarker in vascular remodeling diseases. This study aimed to evaluate the diagnostic performance and prognostic value of serum ADAMTS4 in patients with PAH-CHD.

This study included patients with PAH-CHD, patients with CHD, and healthy controls. Serum ADAMTS4 levels were measured by ELISA. Correlations with clinical parameters were assessed using Spearman's rank correlation. The diagnostic efficacy was evaluated by ROC curve analysis. Univariate and multivariable logistic regression were used to identify independent risk factors associated with the presence of PAH-CHD. PAH-CHD patients were followed up for a median duration of 40.5 months, and Kaplan-Meier and Cox regression analyses were used to analyze prognosis.

Compared with those in CHD patients and healthy controls, serum ADAMTS4 levels were elevated in PAH-CHD patients. ADAMTS4 was positively correlated with NT-proBNP (r = 0.45, p = 0.002), CRP (r = 0.60, p < 0.001), and WHO functional class (r = 0.49, p < 0.001). ROC analysis demonstrated good discriminatory ability for differentiating PAH-CHD from CHD (AUC = 0.78; 95% CI: 0.69-0.87; p < 0.001), with an optimal cutoff value of 42.2 ng/mL. After multivariable adjustment, logistic regression revealed that ADAMTS4 remained an independent factor associated with the presence of PAH-CHD (OR = 1.189; 95% CI: 1.036-1.365; p = 0.014). Kaplan-Meier analysis revealed significantly shorter event-free survival in patients with ≥ 42.2 ng/mL ADAMTS4 than in those with lower levels (log-rank p = 0.046). After multivariable adjustment, Cox regression confirmed ADAMTS4 as an independent predictor of adverse clinical events (HR = 1.038; 95% CI: 1.007-1.071; p = 0.017).

Serum ADAMTS4 is elevated in patients with PAH-CHD and is correlated with disease severity and adverse outcomes. These findings support its utility as a noninvasive serum biomarker for diagnosis, risk stratification and prognostic assessment in PAH-CHD patients.