ObjectivesHeart rate variability (HRV) has gained recognition as a noninvasive marker of autonomic activity. HRV is considered a promising tool in various clinical scenarios. The optimal electrocardiogram (ECG) sampling frequency required to ensure sufficient precision of R–R intervals for HRV analysis has not yet been determined. Here, we aimed to determine the acceptable ECG sampling frequency range by analyzing ECG signals from patients who visited an emergency department with the chief complaint of acute intoxication or overdose.MethodsThe study included 83 adult patients who visited an emergency department with the chief complaint of acute poisoning. The original 1,000-Hz ECG signals were down-sampled to 500-, 250-, 100-, and 50-Hz sampling frequencies with linear interpolation. R–R interval data were analyzed for time-domain, frequency-domain, and nonlinear HRV parameters. Parameters derived from the data on down-sampled frequencies were compared with those derived from the data on 1,000-Hz signals, and Lin's concordance correlation coefficients were calculated.ResultsDown-sampling to 500 or 250 Hz resulted in excellent concordance. Signals down-sampled to 100 Hz produced acceptable results for time-domain analysis and Poincaré plots, but not for frequency-domain analysis. Down-sampling to 50 Hz proved to be unacceptable for both time- and frequency-domain analyses. At 50 Hz, the root-mean-squared successive differences and the power of high frequency tended to have high values and random errors.ConclusionsA 250-Hz sampling frequency would be acceptable for HRV analysis. When frequency-domain analysis is not required, a 100-Hz sampling frequency would also be acceptable.

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We examined the anti-cancer effect of genistein, a soy-derived isoflavone, in human bladder transitional cell carcinoma T24 cells. According to our data, genistein induced G2/M phase arrest of the cell cycle and apoptosis. Genistein down-regulated the levels of cyclin A and cyclin B1, but up-regulated the levels of p21WAF1/CIP1, cyclin-dependent kinase (Cdk) inhibitor, that was complexed with Cdc2 and Cdk2. Furthermore, genistein induced the activation of caspases (caspase-3, -8 and -9), and cleavage of poly (ADP-ribose) polymerase cleavage. However, genistein-induced apoptosis was significantly inhibited by a pan-caspase inhibitor, indicating that the induction of apoptosis by genestein was caspase-dependent. In addition, genistein increased the cytosolic release of cytochrome c by increasing the Bax/Bcl-2 ratio and destroying mitochondria integrity. Moreover, genistein inactivated the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway, while LY294002, a PI3K/Akt inhibitor, increased the apoptosis-inducing effect of genistein. Genistein further increased the accumulation of reactive oxygen species (ROS), which was significantly suppressed by N-acetyl cysteine (NAC), a ROS scavenger, and in particular, NAC prevented genistein-mediated inactivation of PI3K/Akt signaling, G2/M arrest and apoptosis. Therefore, the present results indicated that genistein promoted apoptosis induction in human bladder cancer T24 cells, which was associated with G2/M phase cell cycle arrest via regulation of ROS-dependent PI3K/Akt signaling pathway.

The results show the inhibitory effects of rebamipide on pain production and cartilage degeneration in experimentally induced OA. The suppression of oxidative damage and the restoration of extracellular matrix homeostasis of articular chondrocyte suggest that rebamipide is a potential therapeutic strategy for OA.