Continuous monitoring of pulse waves plays a significant role in reflecting physical conditions and disease diagnosis. However, the current collection equipment cannot simultaneously achieve wearable and continuous monitoring under varying pressure and provide personalized pulse wave monitoring targeted different human bodies. To solve the above problems, this paper proposed a novel wearable and real-time pulse wave monitoring system based on a novel flexible compound sensor. Firstly, a custom-packaged pressure sensor, a signal stabilization structure, and a micro pressurization system make up the flexible compound sensor to complete the stable acquisition of pulse wave signals under continuously varying pressure. Secondly, a real-time algorithm completes the analysis of the trend of the pulse wave peak, which can quickly and accurately locate the best pulse wave for different individuals. Finally, the experimental results show that the wearable system can both realize continuous monitoring and reflecting trend differences and quickly locate the best pulse wave for different individuals with the 95% accuracy. The weight of the whole system is only 52.775 g, the working current is 46 mA, and the power consumption is 160 mW. Its small size and low power consumption meet wearable and portable scenarios, which has significant research value and commercialization prospects.
Acute myocardial infarction (AMI) is a heart disease that seriously threatens human health. Dexmedetomidine (DEX) has a certain protective effect on cardiac injury. This study investigated the cardioprotective effect of DEX and its potential molecular mechanism in vivo and in vitro. The results showed that DEX could significantly increase the viability of hypoxia/reoxygenation (H/R) treated cardiomyocytes and reduce oxidative damage and apoptosis. Further molecular mechanism analysis showed that the above cardiac protective effects may be related to Akt signaling pathway. In addition, the expression of G-Protein Receptor 30 (GPR30) was promoted after H/R treatment. However, knockdown of GPR30 by shRNA significantly counteracted the cardioprotective effect of DEX. Meanwhile, we constructed a rat model of AMI to investigate the role of GPR30 in vivo. The results showed that DEX significantly reduced the infarct size, and GPR30 agonist G1 enhanced the protective effect of DEX on heart. On the contrary, protein kinase B (AKT) inhibitor LY294002 counteracted the protective effect of DEX on heart, suggesting that GPR30 enhanced the protective effect of DEX on ischemia-reperfusion induced heart injury by regulating AKT related pathways. In conclusion, our study provides a potential target for the clinical treatment of AMI.
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