: CA125 is a well-known tumor marker for diagnosis, monitoring, and risk stratification in ovarian cancer. It is not specific for malignant tumors and may be elevated in benign disease. In the past two decades, increasing evidence has emerged suggesting that the plasma level of CA125 can serve as a novel surrogate of heart failure (HF). CA125 in patients with HF is synthesized by epithelial serous cells in response to both mechanical and inflammatory stimuli. In patients with HF, regardless of etiology, CA125 levels correlate with the severity of clinical, hemodynamic, and echocardiographic parameters and with other biomarkers. Elevated CA125 can identify patients at high risk of rehospitalization and mortality, whether short- or long-term. Serial measurements and combination with different pathophysiology biomarkers can provide more accurate prognosis value. It also can guide treatment due to as a robust biomarker of fluid overload and inflammation, particularly for diuretic dose optimization. These properties make it a very promising candidate for risk stratification and treatment guidance of HF.

Melatonin has been shown to protect against ischemia/reperfusion (I/R)‐induced myocardial injury, however, the precise molecular mechanisms have not been fully clarified. The present study was aimed to investigate whether inactivation of Rac1/JNK/Foxo3a/Bim signaling pathway is responsible for the protective effect of melatonin on I/R‐induced myocardial injury. Our results showed that Foxo3a downregulation contributed to the protective effect of melatonin on OGD/R‐induced injury of H9c2 cardiomyoblasts. Melatonin treatment led to a reduced activity of Rac1, which was responsible for Foxo3a downregulation and decreased cell injury in OGD/R‐exposed H9c2 cells. Furthermore, JNK acts as a downstream effector of Rac1 in mediating melatonin‐induced inactivation of Foxo3a/Bim signaling pathway and decreased cell injury in OGD/R‐exposed H9c2 cells. In conclusion, our results indicate that melatonin protects H9c2 cells against OGD/R‐induced injury by inactivating the Rac1/JNK/Foxo3a/Bim signaling pathway. This study provided a novel insight into the protective mechanism of melatonin against I/R‐induced myocardial injury.

Melatonin has been shown to exert protective effect during myocardial ischemia/reperfusion (I/R). However, the underlying mechanism is not completely understood. Using the oxygen-glucose deprivation and reperfusion (OGD/R) model of H9c2 cells in vitro, we found that melatonin alleviated OGD/R-induced H9c2 cell injury via inhibiting Foxo3a/Bim signaling pathway. Inhibition of Rac1 activation contributed to the protective effect of melatonin against OGD/R injury in H9c2 cells. Additionally, melatonin inhibited OGD/R-activated Foxo3a/Bim signaling pathway through inactivation of Rac1. Furthermore, JNK inactivation was responsible for Rac1 inhibition-mediated inactivation of Foxo3a/Bim signaling pathway and decreased cell injury in melatonin-treated H9c2 cells. Taken together, these findings identified a Rac1/JNK/Foxo3a/Bim signaling pathway in melatonin-induced protective effect against OGD/R injury in H9c2 cells. This study provided a novel insight into the protective mechanism of melatonin against myocardial I/R injury.

Introduction. We evaluated the effects of foot reflexology on bodily vital signs. Methods. Randomized controlled trials (RCTs) evaluating the effects of foot reflexology on vital signs were collected for a meta-analysis. Statistical analysis was conducted using RevMan5.4 software and pooled estimates of the effects were reported as mean differences (MDs) with 95% confidence intervals (CIs). Results. Thirteen studies, including 819 patients, met our inclusion criteria. Our results showed that systolic blood pressure (SBP) (MD = -4.62, 95% CI: -5.58 to -3.66; P < 0.00001 ), diastolic blood pressure (DBP) (MD = -3.32, 95% CI: -4.48 to -2.17; P < 0.00001 ), heart rate (HR) (MD = -4.76, 95% CI: -6.49 to -3.04; P < 0.00001 ), respiratory rate (RR) (MD = -0.77, 95% CI: -1.50 to -0.48; P < 0.00001 ), and pulse oxygen saturation (SpO2) (MD = 0.95, 95% CI: 0.39 to 1.52; P = 0.0009 ) showed statistical significance in the foot reflexology group. Conclusions. Short-term followup results showed that foot reflexology exerted positive effects on vital signs, reduced BP, HR, and RR and increased SpO2.