Electron-Ion Coupling Mechanism to Construct Stable Output Performance Nanogenerator.

Recently, triboelectric nanogenerators (TENGs) have been promoted as an effective technique for ambient energy harvesting, given their large power density and high energy conversion efficiency. However, traditional TENGs based on the combination of triboelectrification effect and electrostatic induction have proven susceptible to environmental influence, which intensively restricts their application range. Herein, a new coupling mechanism based on electrostatic induction and ion conduction is proposed to construct flexible stable output performance TENGs (SOP-TENGs). The calcium chloride doped-cellulose nanofibril (CaCl2-CNF) film made of natural carrots was successfully introduced to realize this coupling, resulting from its intrinsic properties as natural nanofibril hydrogel serving as both triboelectric layer and electrode. The coupling of two conductive mechanisms of SOP-TENG was comprehensively investigated through electrical measurements, including the effects of moisture content, relative humidity, and electrode size. In contrast to the conventional hydrogel ionotronic TENGs that require moisture as the carrier for ion transfer and use a hydrogel layer as the electrode, the use of a CaCl2-CNF film (i.e., ion-doped natural hydrogel layer) as a friction layer in the proposed SOP-TENG effectively realizes a superstable electrical output under varying moisture contents and relative humidity due to the compound transfer mechanism of ions and electrons. This new working principle based on the coupling of electrostatic induction and ion conduction opens a wider range of applications for the hydrogel ionotronic TENGs, as the superstable electrical output enables them to be more widely applied in various complex environments to supply energy for low-power electronic devices.

The Interface between Nanoenergy and Self-Powered Electronics.

In recent decades, nanogenerators based on several techniques such as triboelectric effects, piezoelectric effects, or other mechanisms have experienced great developments. The nanoenergy generated by nanogenerators is supposed to be used to overcome the problem of energy supply problems for portable electronics and to be applied to self-powered microsystems including sensors, actuators, integrated circuits, power sources, and so on. Researchers made many attempts to achieve a good solution and have performed many explorations. Massive efforts have been devoted to developing self-powered electronics, such as self-powered communication devices, self-powered human-machine interfaces, and self-powered sensors. To take full advantage of nanoenergy, we need to review the existing applications, look for similarities and differences, and then explore the ways of achieving various self-powered systems with better performance. In this review, the methods of applying nanogenerators in specific circumstances are studied. The applications of nanogenerators are classified into two categories, direct utilization and indirect utilization, according to whether a treatment process is needed. We expect to offer a line of thought for future research on self-powered electronics.

High-density lipoprotein cholesterol and in-hospital mortality in patients with acute aortic dissection.

The association between high-density lipoprotein cholesterol (HDL-C) and mortality in patients with acute aortic dissection (AAD) is unclear. From January 2007 to January 2014, a total of 928 consecutive AAD patients who were admitted within 48 h after the onset of symptoms were enrolled in the study. Patients were divided into two groups according to whether serum HDL-C level was below the normal lower limit or not. The Cox proportional hazard regression model was used to identify the predictive value of HDL-C for in-hospital mortality in patients with AAD. As compared with normal HDL-C group (n=585), low HDL-C group (n=343) had lower levels of systolic blood pressure and hemoglobin and higher levels of leukocyte, alanine aminotransferase, blood glucose, blood urea nitrogen, creatinine and urea acid. Low HDL-C group had significantly higher in-hospital mortality than normal HDL-C group (21.6% vs. 12.6%, log-rank=10.869, P=0.001). After adjustment for baseline variables including demographics and biologic data, the increased risk of in-hospital mortality in low HDL-C group was substantially attenuated and showed no significant difference (adjusted hazard ratio, 1.23; 95% confidence interval, 0.86-1.77; P=0.259). Low HDL-C is strongly but not independently associated with in-hospital mortality in patients with AAD.

CYP2C8-derived epoxyeicosatrienoic acids decrease oxidative stress-induced endothelial apoptosis in development of atherosclerosis: Role of Nrf2 activation.

The aim of the present study is to investigate how cytochrome P450 enzymes (CYP) 2C8-derived epoxyeicosatrienoic acids (EETs) regulate the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and protect against oxidative stress-induced endothelial injuries in the development and progression of atherosclerosis. In this study, cultured human umbilical vein endothelial cells (HUVECs) were transfected with CYP2C8 or pretreated with exogenous EETs (1 µmol/L) before TNF-α (20 ng/mL) stimulation. Apoptosis and intracellular ROS production were determined by flow cytometry. The expression levels of ROS-associated NAD(P)H subunits gp91 and p47, the anti-oxidative enzyme catalase (CAT), Nrf2, heme oxygenase-1 (HO-1) and endothelial nitric oxide synthase (eNOS) were detected by Western blotting. The results showed that CYP2C8-derived EETs decreased apoptosis of HUVECs treated with TNF-α. Pretreatment with 11, 12-EET also significantly blocked TNF-α-induced ROS production. In addition, 11, 12-EET decreased oxidative stress-induced apoptosis. Furthermore, the ability of 11, 12-EET to protect cells against TNF-α-induced apoptosis via oxidative stress was abrogated by transient transfection with Nrf2-specific small interfering RNA (siRNA). In conclusion, CYP2C8-derived EETs prevented TNF-α-induced HUVECs apoptosis via inhibition of oxidative stress associated with the Nrf2 signaling.