A simplified method is presented to fabricate polymer composite electrodes for electrocardiograph (ECGmeasurements. The composite electrode was fabricated by loading a high content of carbon nanotube.(CNTs) and silver nanoparticles (Ag NPs) in polydimethylsiloxane (PDMS). The conductive polymer mixture was prepared by ultrasonically stirring and heat-stirring. Polymer electrodes were fabricated by thedoctor bladetechnique. Two-dimensional electrodes were fabricated to evaluate the effect of thicknesson signal quality. Three polymer electrodes were combined into the ECG electrode patch. The polymerelectrodes were successfully applied in ECG measurements. Continuous measurements for 14 days indi-cated the polymer electrodes are suitable for long-term monitoring. Wearable electrodes were fabricatedwith a laver of gauze embedded by the CNT/Ag-PDMS mixtures. Conductive wires were sewed in thegauze as connectors for the measurement circuit. Three wearable electrodes were sewed into a vest asa measurement module. The ECG measurement results demonstrated that the wearable electrodes arequalified for such medical devices. The CNT-based polymer electrodes are flexible, washable, and suitablefor long-term wear, possessing great promise in practical applications in wearable medical instruments.

Gypenoside XVII (GP-17), a tetracyclic triterpene saponin isolated from the functional
food Gynostemma pentaphyllum, has been demonstrated protective effects against
cerebrovascular and cardiovascular diseases on multiple disease models. In this study,
we established a myocardial infarction (MI) model by ligating the left anterior descending
coronary artery, and explored whether GP-17 prevent myocardial ischemia/
reperfusion (I/R) injuries in mice. Compared with the I/R group, GP-17 significantly
improved the cardiac function, reduced the MI, decreased myocardial pathology, activated
superoxide dismutase and catalase, and reduced the content of lactate dehydrogenase,
creatine kinase, malondialdehyde, and inflammatory factor. The proteomic
analysis showed multiple differential proteins between the GP-17 and I/R groups
enriched in endoplasmic reticulum and mitochondria. Western-Blot showed that GP-
17 significantly decreased the expression of GRP78, ATF6, CHOP, and phosphorylation
of PERK, indicating the inhibition of ERS. GP-17 inhibited the expression of
ATG5, LC3A/B, and BAX, illustrating the suppression of autophagy and apoptosis.
Moreover, both GP-17 and 4-PBA could improve the downregulated Mfn2, meaning
that inhibition of ERS regulated the mitochondrial fusion fission balance, thus protected
the function of mitochondria. In conclusion, we found that GP-17 prevented against myocardial I/R injury by inhibit ERS-induced cell apoptosis, autophagy, oxidative
stress, and mitochondrial division.

Hypokalemia causes ectopic heartbeats, but the mechanisms underlying such
cardiac arrhythmias are not understood. In reduced serum K+ concentrations
that occur under hypokalemia, K2P1 two-pore
domain K+ channels change ion
selectivity and switch to conduct inward leak cation currents, which cause aberrant
depolarization of resting potential and induce spontaneous action potential
of human cardiomyocytes. K2P1 is expressed in the human heart but not in
mouse hearts. We test the hypothesis that K2P1 leak cation channels contribute
to ectopic heartbeats under hypokalemia, by analysis of transgenic mice, which
conditionally express induced K2P1 specifically in hearts, mimicking K2P1
channels in the human heart. Conditional expression of induced K2P1 specifically
in the heart of hypokalemic mice results in multiple types of ventricular
ectopic beats including single and multiple ventricular premature beats as well
as ventricular tachycardia and causes sudden death. In isolated mouse hearts
that express induced K2P1, sustained ventricular fibrillation occurs rapidly after
perfusion with low K+ concentration solutions that mimic hypokalemic conditions.
These observed phenotypes occur rarely in control mice or in the hearts that lack K2P1 expression. K2P1-expressing
mouse cardiomyocytes of transgenic
mice much more frequently fire abnormal single and/or rhythmic spontaneous
action potential in hypokalemic conditions, compared to wild type mouse cardiomyocytes
without K2P1 expression. These findings confirm that K2P1 leak cation
channels induce ventricular ectopic beats and sudden death of transgenic mice
with hypokalemia and imply that K2P1 leak cation channels may play a critical
role in human ectopic heartbeats under hypokalemia.