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The exosome of MSCs derived from human umbilical cord blood (HUCB-MSC) has been reported to have cardioprotective effects on mouse models of acute myocardial infarction (AMI) and cardiomyocyte hypoxia injury, but the exact mechanisms involved require further investigation. This paper aimed to study the role of HUCB-MSC-exosomes in inhibiting ferroptosis to attenuate myocardial injury. Compared with sham or normoxia groups, RT-PCR and western blotting showed that divalent metal transporter 1 (DMT1) expression was significantly increased, and Prussian blue staining, ferrous iron (Fe2+), MDA, and GSH level detection demonstrated that ferroptosis occurred in the infraction myocardium and in cardiomyocyte following hypoxia-induced injury. Overexpression of DMT1 promoted H/R-induced myocardial cell ferroptosis, while knockdown of DMT1 significantly inhibited the ferroptosis. HUCB-MSCs-derived exosomes inhibited ferroptosis and reduced myocardial injury, which was abolished in exosome with miR-23a-3p knockout. Moreover, dual luciferase reporter assay confirmed that DMT1 was a target gene of miR-23a-3p. In conclusion, HUCB-MSCs-exosomes may suppress DMT1 expression by miR-23a-3p to inhibit ferroptosis and attenuate myocardial injury.

Carbon emission trading policy not only reduces carbon emissions but also promotes green technological innovation. This study employs difference-in-difference-in-difference model to assess the impact of China’s carbon emission trading policy on both local and national green technological innovation. Furthermore, the effect of carbon emission trading policy on strategic innovation and substantive innovation is compared. Additionally, a heterogeneity analysis is conducted to examine the green technological innovation behaviours among different types of power enterprises. The results illustrate that after implementing the local pilot policy, green technological innovation patent applications in power enterprises in pilot areas increased by 34.9%. Similarly, following the implementation of the national policy, green technological innovation patent applications in power enterprises increased by 45.2%. Regarding innovation quality, after the implementation of the local pilot policy, power enterprises demonstrated a 25.9% increase in substantive innovation and a 29.9% increase in strategic innovation, respectively. Following the implementation of the national policy, power enterprises exhibited a 21.9% increase in substantive innovation and a 39.2% increase in strategic innovation, respectively. In addition, the carbon emissions trading policy has a positive impact on the green technological innovation of state-owned enterprises and large-scale enterprises. Finally, specific policy implications are proposed to promote green innovation in enterprises.

Objective. Long noncoding RNAs (lncRNAs), including some members of small nucleolar RNA host gene (SNHG), are important regulators in myocardial injury, while the role of SNHG4 in myocardial infarction (MI) is rarely known. This study is aimed at exploring the regulatory role and mechanisms of SNHG4 on MI. Methods. Cellular and rat models of MI were established. The expression of relating genes was measured by qRT-PCR and/or western blot. In vitro, cell viability was detected by MTT assay, and cell apoptosis was assessed by caspase-3 level, Bax/Bcl-2 expression, and/or flow cytometry. The inflammation was evaluated by TNF-α, IL-1β, and IL-6 levels. The myocardial injury in MI rats was evaluated by echocardiography, TTC/HE/MASSON/TUNEL staining, and immunohistochemistry (Ki67). DLR assay was performed to confirm the target relationships. Results. SNHG4 was downregulated in hypoxia-induced H9c2 cells and MI rats, and its overexpression enhanced cell viability and inhibited cell apoptosis and inflammation both in vitro and in vivo. SNHG4 overexpression also decreased infarct and fibrosis areas, relieved pathological changes, and improved heart function in MI rats. In addition, miR-148b-3p was an action target of SNHG4, and its silencing exhibited consistent results with SNHG4 overexpression in vitro. DUSP1 was a target of miR-148b-3p, which inhibited the apoptosis of hypoxia-induced H9c2 cells. Both miR-148b-3p overexpression and DUSP1 silencing weakened the effects of SNHG4 overexpression on protecting H9c2 cells against hypoxia. Conclusions. Overexpression of SNHG4 relieved MI through regulating miR-148b-3p/DUSP1, providing potential therapeutic targets.

BackgroundThe objective of this study was to evaluate the quality of anticoagulation by the time in therapeutic range (TTR) for patients with 12-week INR follow-up interval.Materials and methodsFrom January 2018 to December 2020, a selective group of patients who underwent mechanical valve replacement and followed up at our anticoagulation clinic for adjustment of warfarin dose were enrolled. The incidences of complications of anticoagulation therapy were reported by linearized rates. TTR was calculated by the Rosendaal linear interpolation method.ResultsTwo hundred and seventy-four patients were eligible for this study. The mean age of these patients was 52.8 ± 12.7 years, and 65.7% (180 cases) of them were females. The mean duration of warfarin therapy was 16.7 ± 28.1 months. A total of 1309 INR values were collected, representing 66789 patient days. In this study, the mean TTR was 63.7% ± 18.6%, weekly doses of warfarin were 20.6 ± 6.0 mg/weekly, and the mean monitoring interval for the patient was 53.6 ± 27.1 days. There were 153 cases in good TTR group (TTR ≥ 60%) and 121 cases in poor TTR group (TTR < 60%). The calculated mean TTR in both groups was 42.6% ± 22.1% and 74.8% ± 10.4%, respectively. Compared with the TTR ≥ 60% group, the TTR < 60% group exhibited a more prevalence of female gender ( p = 0.001), atrial fibrillation ( p < 0.001), NYHA ≥ III ( p < 0.001), and lower preoperative left ventricular ejection fraction (LVEF, p = 0.032 ). In multivariate analysis, female gender ( p = 0.023) and atrial fibrillation ( p = 0.011) were associated with TTR < 60%. The incidence of major bleeding and thromboembolic events was 2.7% and 1.1% patient-years, respectively. There was one death which resulted from cerebral hemorrhage. The incidence of death was 0.5% patient-years. The difference in anticoagulation-related complications between the TTR < 60% group and the TTR ≥ 60% group was not statistically significant.ConclusionFor patients with stable international normalized ratio monitoring results who are follow-up at anticoagulation clinics, a 12-week monitoring interval has an acceptable quality of anticoagulation. The female gender and atrial fibrillation were associated with TTR < 60%.

Invasive cardiac lipoma is a rare type of primary cardiac tumor that is composed of adipose tissue but infiltrating the adjacent structures. It is a benign tumor that can cause significant morbidity and mortality due to its size and location within the heart. We describe a giant invasive intracardiac lipoma across atrial wall extending to the ascending aorta and the superior vena cava. This review will provide an overview of invasive cardiac lipoma, including its clinical presentation, diagnosis, and management.

Among patients with rheumatic heart disease (RHD), 45% to 60% present with atrial fibrillation (AF), which is associated with increased rates of thromboembolism, heart failure, and even death. The bipolar radiofrequency ablation (BRFA) combining with mitral valve procedure has been adopted in patients of AF associated with RHD, but evaluations about its effectiveness are still limited. A total of 87 patients with RHD and long persistent AF who had accepted mitral valve replacement concomitant with BRFA were studied. Clinical data were collected to analyze the midterm results of BRFA and evaluate its efficiency. Univariate and multivariate analyses were used to identify the independent factors associated with late AF recurrence. Sixty-six (75.9%) patients maintained sinus rhythm after a mean follow-up of 13.4 ± 5.2 months. Late AF recurrence had been detected in 21 (24.1%) patients, 11 (12.6%) patients were confirmed to be AF, 8 (9.2%) patients were atrial flutter and 2 (2.3%) patients were junctional rhythm. In Multivariate logistic regression analysis, body mass index (BMI) (OR = 1.756, 95% CI = 1.289-2.391, p = 0.000) and early AF recurrence (OR = 5.479, 95% CI = 1.189-25.254, p = 0.029) were independent predictors of late AF recurrence. In addition, left ventricular ejection fraction (LVEF) and New York Heart Association class showed a greater improvement in patients who maintained sinus rhythm than those who experienced late AF recurrence. BRFA is an effective technique for the treatment of long persistent AF associated with RHD during mitral valve replacement. The BMI and early AF recurrence are independent predictors for late AF recurrence. Patients with long-term restoration of sinus rhythm experienced a greater improvement of left ventricular function after BRFA.

Background Many studies have demonstrated that the geometry of the carotid bifurcation enables prediction of blood flow variation associated with atherosclerotic plaque formation. The phase angle between the arterial wall circumferential strain and its instantaneous wall shear stress is known as stress phase angle (SPA). This parameter is used to evaluate hemodynamic factors of atherogenesis. Note that SPA can be numerically computed for the purpose of locating atherosclerosis in different artery geometries. However, there is no experimental data to verify its role in the location of atherosclerosis in different artery geometries. In this study, we use an ultrasonic biomechanical method to experimentally evaluate the role of SPA for locating atherosclerosis in carotid bifurcation. Results For carotid anthropomorphic vascular phantom experiments, the SPAs of common carotid arteries (CCAs), external carotid arteries (ECAs) and internal carotid arteries (ICAs) are − 148.53 ± 6.92°, − 153.95 ± 5.11°, and − 238.69 ± 1.72°, respectively. The corresponding SPAs are − 173.47 ± 0.065°, − 115.57 ± 4.83° and − 233.9 ± 8.12° for the polyvinyl alcohol (PVA-c) phantoms. In vivo mouse experiments indicated that the wall shear stress and circumferential strain were out of phase in the ICAs (− 280.08 ± 13.12°) to a greater extent as compared to CCAs (− 141.97 ± 8.03°) and ECAs (− 170.07 ± 9.24°). Conclusions The results suggested that SPA may be a useful indicator to locate the atherosclerosis position in carotid bifurcation.

Bisphenol A (BPA) is a widely used industrial chemical with potential endocrine‐disrupting effects on metabolic processes. This study investigates the impact of BPA on hepatic function and transcriptional regulation in mouse livers and AML12 cells. Male mice were exposed to low (5 g/kg) and high (50 g/kg) doses of BPA for six weeks. Transcriptomic analysis was performed on liver tissues, and histological examinations were conducted. AML12 cells were treated with varying BPA concentrations, and PPARG transcriptional activity was assessed using a luciferase reporter assay. Additionally, molecular docking, molecular dynamics (MD) simulations, drug affinity responsive target stability (DARTS), cellular thermal shift assay (CETSA), MM‐PBSA calculations, and multi‐species protein structure comparative analysis were employed to analyse the interaction between BPA and PPARG. Transcriptomic analysis revealed a decrease in differentially expressed genes with higher BPA doses, with low‐dose exposure significantly downregulating hepatic Cpt1a mRNA levels. Histological examination indicated lipid vacuole formation at high doses without collagen deposition. BPA consistently inhibited PPARG activity in both MCF7 cells and mouse livers. BPA exposure disrupts hepatic lipid metabolism and PPARG activity, highlighting its role as an endocrine disruptor. Further research is needed to elucidate the long‐term effects of BPA on liver health.

BackgroundHigh‐sugar, high‐fat diets (HSDFD) can lead to hepatic dysfunction, but the molecular mechanisms underlying protective compounds like sesamin remain unclear MethodsWe employed a multi‐faceted approach combining in silico and in vivo techniques. Utilizing the AlphaFold database, we screened multi‐species proteomes to identify potential sesamin targets. Molecular dynamics simulations and MM‐PBSA analysis were used to characterize sesamin‐protein interactions. In vivo studies included single‐cell RNA sequencing of hepatocytes from HSDFD‐fed mice. We validated our findings using cellular thermal shift assays (CETSA), drug affinity responsive target stability (DARTS) assays, Western blotting, and qPCR. ResultsHSDFD induced significant redistribution of hepatocyte subpopulations with high CYP1A2 abundance. Computational analysis identified CYP1A2 as a direct target of sesamin, with species‐specific interaction patterns. Sesamin exhibited stable binding to CYP1A2, modulating its activity through subtle conformational changes. Key residues F451 and I386 were crucial for sesamin's regulation of CYP1A2‐mediated ROS production. Sesamin supplementation ameliorated HSDFD‐induced hepatic dysfunction by modulating fatty acid metabolism and oxidative stress responses. ConclusionOur study unveils CYP1A2 as a key molecular target of sesamin in HSDFD‐induced hepatic dysfunction, providing new insights into potential therapeutic strategies for metabolic liver disorders.

Orofacial clefts are among the most common congenital craniofacial abnormalities, yet accurate prenatal detection remains challenging due to the scarcity of experienced specialists and the relative rarity of the condition. Early and reliable diagnosis is essential to enable timely clinical intervention and reduce associated morbidity. Here we show that an artificial intelligence system, trained on over 45,139 ultrasound images from 9,215 fetuses across 22 hospitals, can diagnose fetal orofacial clefts with sensitivity and specificity exceeding 93% and 95% respectively, matching the performance of senior radiologists and substantially outperforming junior radiologists. When used as a medical copilot, the system raises junior radiologists' sensitivity by more than 6 %. Beyond direct diagnostic assistance, the system also accelerates the development of clinical expertise. A pilot study involving 24 radiologists and trainees demonstrated that the model can improve the expertise development for rare conditions. This dual-purpose approach offers a scalable solution for improving both diagnostic accuracy and specialist training in settings where experienced radiologists are scarce.