In this study, the concept of polymer electrodes integrated with a wireless electrocardiogram (ECG) system was described. Polymer electrodes for long-term ECG measurements were fabricated by loading high content of carbon nanotubes (CNTs) in polydimethylsiloxane. Silver nanoparticles (Ag NPs) were added to increase the flexibility of the polymer and the conductivity of the electrode. An ECG electrode patch was fabricated by integrating the electrodes with an adhesive polydimethylsiloxane (aPDMS) layer. Holes in the electrode filled with aPDMS can enable robust contact between the electrode and skin, reducing motion artifacts. A wireless ECG measurement system was developed and adapted to the polymer electrodes. The polymer electrodes combined with the measurement system were successfully applied in wireless, long-term recording of ECG signals. An eleven-day continuous test showed that the ECG signal did not degrade over time. The results of attach/detach tests demonstrated that the ECG signal was affected by motion artifacts after six attach/detach cycles. The electrodes produced are flexible and exhibit good ECG performance, and therefore can be used in wearable medical monitoring systems. The approach proposed in this study holds significant promise for commercial application in medical fields.
SUMMARYBackground: Sympathetic activation and parasympathetic withdrawal are important characteristics of heart failure. Recent studies demonstrate that galanin reduces the discharge of acetylcholine and inhibits vagal bradycardia by acting on galanin receptor type 1 (GalR1). We speculated that blocking GalR1 is beneficial for heart failure. Methods: Rats with heart failure were induced by myocardial infarction. The rats were injected intraperitoneally with galanin receptor antagonist M40 solution (30 nmol/kg) or saline for 4 weeks. Cardiac function was assessed by echocardiography and brain natriuretic peptide (BNP) in plasma. The ratio of heart weight to body weight (HW/BW), hematoxylin-eosin (HE), and Masson trichrome stain was used to evaluate cardiac remodeling. Tumor necrosis factor-a (TNF-a), interleukin 6 (IL-6) in plasma, and sarco(endo)plasmic reticulum Ca 2+ -ATPase
SummaryVagus nerve stimulation (VNS), targeting the imbalanced autonomic nervous system, is a promising therapeutic approach for chronic heart failure (HF). Moreover, calcium cycling is an important part of cardiac excitation-contraction coupling (ECC), which also participates in the antiarrhythmic effects of VNS. We hypothesized that low-level VNS (LL-VNS) could improve cardiac function by regulation of intracellular calcium handling properties. The experimental HF model was established by ligation of the left anterior descending coronary artery (LAD). Thirty-two male Sprague-Dawley rats were divided into 3 groups as follows; control group (sham operated without coronary ligation, n = 10), HF-VNS group (HF rats with VNS, n = 12), and HF-SS group (HF rats with sham nerve stimulation, n = 10). After 8 weeks of treatment, LL-VNS significantly improved left ventricular ejection fraction (LVEF) and attenuated myocardial interstitial fibrosis in the HF-VNS group compared with the HF-SS group. Elevated plasma norepinephrine and dopamine, but not epinephrine, were partially reduced by LL-VNS. Additionally, LL-VNS restored the protein and mRNA levels of sarcoplasmic reticulum Ca 2+ ATPase (SERCA2a), Na + -Ca 2+ exchanger 1 (NCX1), and phospholamban (PLB) whereas the expression of ryanodine receptor 2 (RyR2) as well as mRNA level was unaffected. Thus, our study results suggest that the improvement of cardiac performance by LL-VNS is accompanied by the reversal of dysfunctional calcium handling properties including SERCA2a, NCX1, and PLB which may be a potential molecular mechanism of VNS for HF. (Int Heart J 2016; 57: 350-355)
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