Search

Time-frequency domain reflection (TFDR) method has the advantages of maturity, convenience and high resolution, so it is widely applied to locate defects in various cables. To ensure the fracture defect of the instrumentation and control (I&C) cable can be effectively discriminated and precisely located in nuclear power plant (NPP), an improved TFDR method is proposed by intervening thermal stress in this paper. Subsequently, different degrees of fracture defects are simulated in a 50-meter multi-core I&C cable, and traditional TFDR and improved TFDR methods are used for detection and verification. Comparing the detection results of both, the peak localization of improved TFDR method for weak defect fracture is improved to 0.2, which is 2.5 times of the traditional TFDR method, and the localization error rate is less than 2.5%. Compared to the traditional TFDR method, improved TFDR method utilizes the thermal stress fluctuation variance curve as the basis for defect identification, the identification power of weak fracture defects can be substantially improved. The original localization distance can be corrected to improves the accuracy of weak fracture damage in improved TFDR method. So the effective identification and localization of weak defects can be further achieved in improved TFDR method.

Mitochondrial dysfunctions are responsible for myocardial injury upon ischemia/reperfusion (I/R), and mitochondrial E3 ubiquitin ligase 1 (Mul1) plays an important role in maintaining mitochondrial functions. This study aims to explore the function of Mull in myocardial I/R injury and the underlying mechanisms. The Sprague-Dawley rat hearts were subjected to 1 h of ischemia plus 3 h of reperfusion, which showed the I/R injury (increase in infarct size and creatine kinase release) and the elevated total and mitochondrial protein levels of Mul1 and p53 accompanied by the enhanced interactions between Mul1 and p53 as well as p53 and small a ubiquitin-like modifier (SUMO1). Consistently, hypoxia/reoxygenation (H/R) treated cardiac (H9c2) cells displayed cellular injury (apoptosis and necrosis), upregulation of total and mitochondrial protein levels of Mul1 and p53, and enhanced interactions between p53 and SUMO1 concomitant with mitochondrial dysfunctions (an increase in mitochondrial membrane potential and reactive oxygen species production with a decrease in ATP production); these phenomena were attenuated by knockdown of Mul1 expression. Based on these observations, we conclude that a novel role of Mul1 has been identified in the myocardial mitochondria, where Mul1 stabilizes and activates p53 through its function of SUMOylation following I/R, leading to p53-mediated mitochondrial dysfunction and cell death. Key words: ischemia/reperfusion, myocardial injury, mitochondrial E3 ubiquitin ligase 1, p53, SUMOylation, hypoxia/reoxygenation, mitochondria. Les dysfonctionnements mitochondriaux sont responsables de lesions myocardiques lors de l'ischemie/reperfusion (I/R) et l'E3 ubiquitine ligase mitochondriale 1 (Mul1) joue un role important dans le maintien du fonctionnement des mitochondries. Cette etude portait sur le fonctionnement de la Mul1 dans les lesions d'I/R myocardiques et les modes d'action sous-jacents. Nous avons procede a une ischemie d'une heure suivie d'une reperfusion de trois heures sur des creurs de rats Sprague-Dawley, et observe la presence de lesions d'I/R (augmentation de la taille de l'infarctus et liberation de creatine kinase), l'augmentation des taux de Mul1 et de p53 en proteines totales et mitochondrials, accompagnees de l'augmentation des interactions entre la Mul1 et le p53, ainsi qu'entre le p53 et le petit modificateur ressemblant a l'ubiquitine (ou SUMO1 pour << small ubiquitin-like modifier >>). Les cellules cardiaques H9c2 soumises a l'hypoxie/reoxygenation (H/R) presentaient systematiquement des lesions cellulaires (apoptose et necrose), une regulation a la hausse des taux de Mul1 et de p53 en proteines totales et mitochondriales, avec une augmentation des interactions entre le p53 et le SUMO1 en concomitance avec des dysfonctionnements mitochondriaux (augmentation du potentiel transmembranaire mitochondrial et de la production de derives reactifs de l'oxygene, avec une diminution de la production d'ATP); ces phenomenes s'attenuaient avec la repression de l'expression (<< knockdown >>) du gene Mul1. Sur la foi de ces observations, nous en arrivons a la conclusion que nous avons cerne un nouveau role du gene Mul1 dans la mitochondrie myocardique, par lequel le gene Mul1 entraine une stabilisation et une activation de p53 par l'intermediaire de sa fonction de<< SUMOylation>>consecutive a l'I/R et menant a des dysfonctionnements mitochondriaux et a une mort cellulaire medies par le p53. [Traduit par la Redaction] Mots-cles : ischemie/reperfusion, lesions myocardiques, E3 ubiquitine ligase mitochondriale 1, p53, SUMOylation, hypoxie/ reoxygenation, mitochondrie., Introduction Multiple mechanisms including energy metabolic disorders, calcium overload, oxidative stress, and inflammation are involved in various cardiovascular disorders (Anupama et al. 2018; Kiyuna et al. 2018), all of which [...]