Aims: Irradiation is an effective treatment for tumors but has been associated with cardiac dysfunction. However, the precise mechanisms remain incompletely elucidated. This study investigated the long-term cardiac damage associated with abdominal irradiation and explored possible mechanisms.Methods and Results: Wild-type C57BL6/J mice were divided into two groups: untreated controls (Con) and treatment group receiving 15 Gy of abdominal gamma irradiation (AIR). Both groups received normal feeding for 12 months. The AIR group showed reductions in left ventricular ejection fraction (LVEF), fractional shortening (FS), left ventricular end-diastolic internal diameter (LVID; d), left ventricular end-diastolic volume (LV Vol. diastolic volume (LV Vol; d) and mitral transtricuspid flow late diastolic filling velocity (MV A). It also showed increased fibrosis, reduced conduction velocity and increased conduction heterogeneity. Non-targeted metabolomics showed the differential metabolites were mainly from amino acid metabolism. Further KEGG pathway annotation and enrichment analysis revealed that abnormalities in arginine and proline metabolism, lysine degradation, d-arginine and d-ornithine metabolism, alanine, aspartate and glutamate metabolism, and arginine biosynthesis.Conclusion: Abdominal irradiation causes long-term damage to the non-irradiated heart, as reflected by electrical and structural remodeling and mechanical dysfunction associated with abnormal amino acid biosynthesis and metabolism.

Mitochondria-dependent ferroptosis plays an important role in the pathogenesis of doxorubicin (DOX)-induced cardiotoxicity (DIC), which remains a clinical challenge due to the lack of effective interventions. Cerium oxide (CeO2), a representative nanozyme, has attracted much attention because of its antioxidant properties. This study evaluated CeO2-based nanozymes for the prevention and treatment of DIC in vitro and in vivo by adding nanoparticles (NPs), which were synthesized by biomineralization, to the culture or giving them to the mice, and the ferroptosis-specific inhibitor ferrostatin-1 (Fer-1) was used as control. The prepared NPs exhibited an excellent antioxidant response and glutathione peroxidase 4 (GPX4)-depended bioregulation, with the additional merits of bio-clearance and long retention in the heart. The experiments showed that NP treatment could significantly reverse myocardial structural and electrical remodeling, and reduce myocardial necrosis. These cardioprotective therapeutic effects were associated with their ability to alleviate oxidative stress, mitochondrial lipid peroxidation, and mitochondrial membrane potential damage, with a superior efficiency to the Fer-1. The study also found that the NPs significantly restored the expression of GPX4 and mitochondrial-associated proteins, thereby restoring mitochondria-dependent ferroptosis. Therefore, the study provides some insights into the role of ferroptosis in DIC. It also shows that CeO2-based nanozymes could be a promising prevention and treatment candidate as a novel cardiomyocyte ferroptosis protector to mitigate DIC and improve prognosis and quality of life in cancer patients.

As an important detection means of partial discharges, range sensor is widely used in power system in China. Due to the complex and open environment around covered conductor overhead distribution networks, misjudgement and leakage in long-distance of traditional ultrasonic sensors often occur. Aiming at this problem, an range sensor with high sensitivity and directivity is designed in this paper. In this paper, the theoretical model of the ultrasonic screening can is established by COMSOL simulation software, and the structure of the screening can is designed reasonably by analyzing the concentr-ation and directivity of the sound field of the model. In addition, based on the ultrasonic characteristics generated by partial discharge of overhead insulation wire, the ultrasonic probe with a central frequency of 40kHz was selected, and an amplification and filtering circuit was designed to reasonably improve the signal-to-noise ratio of ultrasonic detection signal. The results of laboratory test and field application show that the sensor can accurately detect and locate the partial discharge of covered conductor overhead distribution networks.

BackgroundDoxorubicin is a widely used cytotoxic chemotherapy agent for treating different malignancies. However, its use is associated with dose‐dependent cardiotoxicity, causing irreversible myocardial damage and significantly reducing the patient's quality of life and survival. In this study, an animal model of doxorubicin‐induced cardiomyopathy was used to investigate the pathogenesis of doxorubicin‐induced myocardial injury. This study also investigated a possible treatment strategy for alleviating myocardial injury through resveratrol therapy in vitro.MethodsAdult male C57BL/6J mice were randomly divided into a control group and a doxorubicin group. Body weight, echocardiography, surface electrocardiogram, and myocardial histomorphology were measured. The mechanisms of doxorubicin cardiotoxicity in H9c2 cell lines were explored by comparing three groups (phosphate‐buffered saline, doxorubicin, and doxorubicin with resveratrol).ResultsCompared to the control group, the doxorubicin group showed a lower body weight and higher systolic arterial pressure, associated with reduced left ventricular ejection fraction and left ventricular fractional shortening, prolonged PR interval, and QT interval. These abnormalities were associated with vacuolation and increased disorder in the mitochondria of cardiomyocytes, increased protein expression levels of α‐smooth muscle actin and caspase 3, and reduced protein expression levels of Mitofusin2 (MFN2) and Sirtuin1 (SIRT1). Compared to the doxorubicin group, doxorubicin + resveratrol treatment reduced caspase 3 and manganese superoxide dismutase, and increased MFN2 and SIRT1 expression levels.ConclusionDoxorubicin toxicity leads to abnormal mitochondrial morphology and dysfunction in cardiomyocytes and induces apoptosis by interfering with mitochondrial fusion. Resveratrol ameliorates doxorubicin‐induced cardiotoxicity by activating SIRT1/MFN2 to improve mitochondria function.