In this paper, a printed monopole antenna design for WiMAX/WLAN applications in cable-free self-positioning seismograph nodes is proposed. Great improvements were achieved in miniaturizing the antenna and in widening the narrow bandwidth of the high-frequency band. The antenna was fed by a microstrip gradient line and consisted of a triangle, an inverted-F shape, and an M-shaped structure, which was rotated 90° counterclockwise to form a surface-radiating patch. This structure effectively widened the operating bandwidth of the antenna. Excitation led to the generation of two impedance bands of 2.39–2.49 and 4.26–7.99 GHz for a voltage standing wave ratio of less than 2. The two impedance bandwidths were 100 MHz, i.e., 4.08% relative to the center frequency of 2.45 GHz, and 3730 MHz, i.e., 64.31% relative to the center frequency of 5.80 GHz, covering the WiMAX high-frequency band (5.25–5.85 GHz) and the WLAN band (2.4/5.2/5.8). This article describes the design details of the antenna and presents the results of both simulations and experiments that show good agreement. The proposed antenna meets the field-work requirements of cable-less seismograph nodes.

Hyperglycaemia is associated with the development of cardiac vascular disease. Resveratrol (RES) is a naturally occurring polyphenolic compound that possesses many biological properties, including anti-inflammatory properties and antioxidation functions. Our study aimed to explore the RES’s protective roles on high glucose (HG)-induced H9c2 cells and the underlying mechanisms. Small-molecule inhibitors, western blotting (WB), as well as reverse-transcription PCR (RT-PCR) were employed to investigate the mechanisms underlying HG-induced damage in H9c2 cells. RES (40 μg/mL) treatment significantly alleviated HG-induced cardiac hypertrophy and cardiac dysfunction. RES abated the HG‐induced increase in the levels of extracellular matrix (ECM) components and inflammatory cytokines, reducing ECM accumulation and inflammatory responses. Additionally, RES administration prevented HG‐induced mitochondrion‐mediated cardiac apoptosis of myocardial cells. In terms of mechanisms, we demonstrated that RES ameliorated the HG‐induced overexpression of receptor for advanced glycation endproducts (RAGE) and downregulation of NF-κB signalling. Moreover, RES inhibited HG‐induced cardiac fibrosis by inhibiting transforming growth factor beta 1 (TGF‐β1)/Smad3‐mediated ECM synthesis in cultured H9c2 cardiomyocytes. Further studies revealed that the effects of RES against HG‐induced upregulation of NF-κB and TGF‐β1/Smad3 pathways were similar to those of FPS-ZM1, a RAGE inhibitor. Collectively, the results implied that RES might help alleviate HG‐induced cardiotoxicity via RAGE‐dependent downregulation of the NF-κB and TGF‐β/Smad3 pathways. This study provided evidence that RES can be developed as a promising cardioprotective drug.

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