The Normal zone propagation velocity (NZPV) of a double-layer second generation high temperature superconducting wire manufactured by American Superconductor has been measured by electrical and thermal methods, and the results have been compared and discussed. The NZPV values determined by the voltage traces are ranging from 3.8 mm/s at 0.4 I _c to 19.2 mm/s at 0.9 I _c ; while from 5.9 to 18.3 mm/s by the temperature traces. NZPV determined by these two approaches agrees well with each other. Also, NZPV of double-layer YBCO tape is close to that of conventional single-layer superconducting tape.

This study aims to investigate the therapeutic potential of Flavagline3 (FL3) in mitigating myocardial ischemia-reperfusion (IR) injury, with a specific focus on its regulatory effects on mitochondrial fusion, mitochondrial-endoplasmic reticulum (ER) interactions, and calcium homeostasis in cardiomyocytes. Using a well-established myocardial IR injury model in mice and primary cardiomyocytes treated with FL3, the study assessed its impact on mitochondrial dynamics and intracellular signaling processes. The results demonstrated that FL3 effectively reduced myocardial apoptosis, infarct size, and cardiac dysfunction caused by IR injury. Mechanistically, FL3 promoted mitochondrial fusion in a mitofusin1 (MFN1)-dependent manner, preserving mitochondrial function under stress conditions and enhancing cellular resilience. Furthermore, FL3 facilitated mitochondrial-ER crosstalk, which played a critical role in modulating intracellular calcium levels by optimizing the transfer of calcium ions between these two organelles. This balanced regulation of mitochondrial dynamics and calcium homeostasis was associated with improved survival and functionality of cardiomyocytes following IR injury. These findings suggest that FL3 exerts robust cardioprotective effects through its ability to promote mitochondrial fusion, enhance mitochondrial-ER interactions, and maintain calcium homeostasis. As a result, FL3 holds promise as a potential therapeutic agent for reducing myocardial damage and dysfunction associated with IR injury, offering valuable insights into novel approaches for cardioprotection.

Background: Atrial fibrillation (AF) is a prevalent and chronic cardiovascular disorder associated with various pathophysiological alterations, including atrial electrical and structural remodeling, disrupted calcium handling, autonomic nervous system dysfunction, aberrant energy metabolism, and immune dysregulation. Emerging evidence suggests that long non-coding RNAs (lncRNAs) play a significant role in the pathogenesis of AF. Objective: This discussion aims to elucidate the involvement of AF-related lncRNAs, with a specific focus on their role as miRNA sponges that modulate crucial signaling pathways, contributing to the progression of AF. We also address current limitations in AF-related lncRNA research and explore potential future directions in this field. Additionally, we summarize feasible strategies and promising delivery systems for targeting lncRNAs in AF therapy. Conclusion: In conclusion, targeting AF-related lncRNAs holds substantial promise for future investigations and represents a potential therapeutic avenue for managing AF.

Managing recurrent atrial flutter (AFL) following radiofrequency ablation (RFA) for atrial fibrillation (AF) poses significant clinical challenges. We report an 82-year-old male with mirror-image dextrocardia who developed AFL post-AF ablation. During the redo procedure, vein of Marshall ethanol infusion (VOM-Et) was employed as the initial intervention, successfully terminating the mitral isthmus (MI)-dependent AFL and transitioning into cavotricuspid isthmus (CTI)-dependent AFL during ethanol infusion. Subsequent ablation restored sinus rhythm. Using VOM-EI as the initial intervention in patients with recurrent AFL is a feasible and safe approach, and to our knowledge, this represents the first reported case of VOM-EI in a patient with recurrent AFL in the setting of dextrocardia.

Background: Abnormal uterine bleeding is a clinically important but often overlooked concern during antithrombotic therapy, particularly in cardiovascular care where anticoagulant and antiplatelet regimens are used. Objective: To describe paired menstrual changes during cardiovascular antithrombotic therapy and to explore documented increased or prolonged bleeding across treatment classes and observed regimens. Methods: This prospective observational paired clinical follow-up study included 50 menstruating women aged 18–55 years with regular menses who received antithrombotic therapy for cardiovascular conditions. Source records specified monthly follow-up and at least 3 months of anticipated treatment. Primary outcomes were paired changes in menstrual-cycle category and menstrual duration; documented increased or prolonged bleeding and variation across observed regimens were secondary exploratory outcomes. Results: Abnormal menstrual-cycle categories increased from 8/50 (16.0%) to 14/50 (28.0%), and prolonged menses increased from 2/49 (4.1%) to 8/49 (16.3%); both exact McNemar P=0.031. Documented increased or prolonged bleeding was recorded in 17/46 evaluable participants (37.0%). Menstrual-related healthcare use or absence was more frequent among those with documented bleeding than among those without it (9/17 vs 4/29; Fisher P = 0.007). The proportion with documented bleeding varied across seven observed regimens (P=0.006) and was highest among rivaroxaban recipients (13/19, 68.4%). Conclusions: Menstrual changes and bleeding-related clinical burden were observed during follow-up in women receiving antithrombotic therapy for cardiovascular conditions. The proportion with documented bleeding varied across observed regimens and was highest among rivaroxaban recipients. Larger prospective studies using standardized menstrual outcome measures are needed to evaluate between-regimen differences.