Architectural Design of a Multichannel Porous Carbon Fiber for Efficient Electromagnetic Microwave Absorption.

An ingenious microstructure of electromagnetic microwave absorption materials is crucial to achieve strong absorption and a broad bandwidth. Herein, one-dimensional (1D) carbon fibers with implantation of zero-dimensional (0D) ZIF-8-derived carbon frameworks and construction of a three-dimensional (3D) microcosmic multichannel porous structure are fabricated by electro-blown spinning, solvent-thermal reaction, and high-temperature pyrolysis techniques. The 1D carbon fiber skeleton with a multichannel structure provides a direct axial conductive pathway for charge transport, which plays an important role in dielectric loss. The 0D surface carbon frameworks offer plenty of heterogeneous interfaces to trigger intensive interfacial polarization loss and act as dihedral angles for microwave scattering. The 3D microcosmic multichannel pores can not only generate multiple reflections as much as possible to dissipate electromagnetic microwave energy but also supply huge interior cavities to improve impedance matching. Thanks to the synergistic effect of a strong electrically conductive pathway for enhancing the conductive loss, a plenteous heterogeneous interface for triggering intensive interfacial polarization loss, microcosmic multichannel pores for generating multiple reflections and improving impedance matching, and N and O atom doping for inducing dipole polarization, the optimal sample with an ingenious microstructure delivers an excellent absorption performance of a minimum reflection loss of -35.5 dB at a thickness of 5.0 mm and an effective absorption bandwidth of 6.72 GHz (10.96-17.68 GHz) at a thickness of 2.0 mm. Such a well-designed multichannel porous carbon fiber may pave the way for the exploitation of high-performance microwave absorbing materials.

Periplocymarin alleviates pathological cardiac hypertrophy via inhibiting the JAK2/STAT3 signalling pathway.

Pathological cardiac hypertrophy is the most important risk factor for developing chronic heart failure. Therefore, the discovery of novel agents for treating pathological cardiac hypertrophy remains urgent. In the present study, we examined the therapeutic effect and mechanism of periplocymarin (PM)-mediated protection against pathological cardiac hypertrophy using angiotensinII (AngII)-stimulated cardiac hypertrophy in H9c2 cells and transverse aortic constriction (TAC)-induced cardiac hypertrophy in mice. In vitro, PM treatment significantly reduced the surface area of H9c2 cells and expressions of hypertrophy-related proteins. Meanwhile, PM markedly down-regulated AngII-induced translocation of p-STAT3 into the nuclei and enhanced the phosphorylation levels of JAK2 and STAT3 proteins. The STAT3 specific inhibitor S3I-201 or siRNA-mediated depleted expression could alleviate AngII-induced cardiac hypertrophy in H9c2 cells following PM treatment; however, PM failed to reduce the expressions of hypertrophy-related proteins and phosphorylated STAT3 in STAT3-overexpressing cells, indicating that PM protected against AngII-induced cardiac hypertrophy by modulating STAT3 signalling. In vivo, PM reversed TAC-induced cardiac hypertrophy, as determined by down-regulating ratios of heart weight to body weight (HW/BW), heart weight to tibial length (HW/TL) and expressions of hypertrophy-related proteins accompanied by the inhibition of the JAK2/STAT3 pathway. These results revealed that PM could effectively protect the cardiac structure and function in experimental models of pathological cardiac hypertrophy by inhibiting the JAK2/STAT3 signalling pathway. PM is expected to be a potential lead compound of the novel agents for treating pathological cardiac hypertrophy.

Effect of high temperature stress on heat shock protein expression and antioxidant enzyme activity of two morphs of the mud crab Scylla paramamosain.

The present study aimed to investigate the effect rapid temperature change from moderate temperature to high temperatures on heat shock protein (HSP) expression and antioxidant enzyme activities in mud crabs. Two mud crabs, one with one spine on the outer margin of the carpus of cheliped (Sp1) and another with two spines (Sp2), were acclimated at 25 °C and then transferred to a 33 °C environment, and HSP expression and antioxidant enzyme activity were assessed. HSP70 and HSP60 were markedly up-regulated in the gills and hepatopancreas of Sp1 and Sp2 after exposure to 35 °C. Exposure to 35 °C also significantly increased superoxide dismutase and catalase activity in the gills of Sp1 and Sp2, with transient changes in hepatopancreas. Apart from changes in antioxidant enzyme activities, HSPs were highly up-regulated after exposure to 37 °C, especially for HSP70. Gill HSP70 expression in Sp2 was 6.1 folds that of the control after 24 h of exposure to 37 °C, and 9.2 folds that of Sp1. Moreover, exposure to 37 °C further up-regulated HSP70 in the hepatopancreas of Sp1, compared to that in Sp2. Hence, HSPs play important roles in thermotolerance in S. paramamosain and Sp1 might have a stronger tolerance to hyperthermal stress than Sp2.

Qili Qiangxin, a compound herbal medicine formula, alleviates hypoxia-reoxygenation-induced apoptotic and autophagic cell death via suppression of ROS/AMPK/mTOR pathway in vitro.

OBJECTIVE: Qili Qiangxin (QLQX), a compound herbal medicine formula, is used effectively to treat congestive heart failure in China. However, the molecular mechanisms of the cardioprotective effect are still unclear. This study explores the cardioprotective effect and mechanism of QLQX using the hypoxia-reoxygenation (H/R)-induced myocardial injury model. METHODS: The main chemical constituents of QLQX were analyzed using high-performance liquid chromatography-evaporative light-scattering detection. The model of H/R-induced myocardial injury in H9c2 cells was developed to simulate myocardial ischemia-reperfusion injury. Apoptosis, autophagy, and generation of reactive oxygen species (ROS) were measured to assess the protective effect of QLQX. Proteins related to autophagy, apoptosis and signalling pathways were detected using Western blotting. RESULTS: Apoptosis, autophagy and the excessive production of ROS induced by H/R were significantly reduced after treating the H9c2 cells with QLQX. QLQX treatment at concentrations of 50 and 250 µg/mL caused significant reduction in the levels of LC3II and p62 degradation (P < 0.05), and also suppressed the AMPK/mTOR signalling pathway. Furthermore, the AMPK inhibitor Compound C (at 0.5 µmol/L), and QLQX (250 µg/mL) significantly inhibited H/R-induced autophagy and apoptosis (P < 0.01), while AICAR (an AMPK activator, at 0.5 mmol/L) increased cardiomyocyte apoptosis and autophagy and abolished the anti-apoptotic effect of QLQX. Similar phenomena were also observed on the expressions of apoptotic and autophagic proteins, demonstrating that QLQX reduced the apoptosis and autophagy in the H/R-induced injury model via inhibiting the AMPK/mTOR pathway. Moreover, ROS scavenger, N-Acetyl-L-cysteine (NAC, at 2.5 mmol/L), significantly reduced H/R-triggered cell apoptosis and autophagy (P < 0.01). Meanwhile, NAC treatment down-regulated the ratio of phosphorylation of AMPK/AMPK (P < 0.01), which showed a similar effect to QLQX. CONCLUSION: QLQX plays a cardioprotective role by alleviating apoptotic and autophagic cell death through inhibition of the ROS/AMPK/mTOR signalling pathway.