This paper presents an optically transparent active bandstop frequency selective surface (FSS) with wideband tunability of two resonance frequencies using the concept of miniaturized element FSS (MEFSS). The proposed design consists of metallic square loop arrays on a new optically transparent substrate as the top layer, a glass interlayer, and periodic patterns of cross dipoles on the substrate as the bottom layer. Two kinds of resonant elements loaded with varactors and the designed bias networks achieve two independent tunable stopbands. The proposed FSS has two large tuning ranges, one is from 1.20 GHz to 2.63 GHz and another is from 2.0 GHz to 5.9 GHz (75% and 99% with respect to the center frequency, respectively). The wideband dual-tuning mechanism is theoretically analyzed and demonstrated by deriving its equivalent circuit (EC) model. The experiment results exhibit reasonable agreement with the numerical simulation responses. This proposed design, with low profile, angular stability, polarization insensitivity, optical transparency, and wideband dual-tunability can play an important role in manipulating electromagnetic wave propagation for manifold applications.
Background/Aims: Cardiac sympathetic afferent reflex (CSAR) enhancement contributes to exaggerated sympathetic activation in chronic heart failure (CHF). The current study aimed to investigate the roles of angiotensin (Ang)-(1-7) in CSAR modulation and sympathetic activation and Ang-(1-7) signaling pathway in paraventricular nucleus of CHF rats. Methods: CHF was induced by coronary artery ligation. Responses of renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) to epicardial application of capsaicin were used to evaluate CSAR in rats with anesthesia. Results: Ang-(1-7) increased RSNA, MAP, CSAR activity, cAMP level, NAD(P)H oxidase activity and superoxide anion level more significantly in CHF than in sham-operated rats, while Mas receptor antagonist A-779 had the opposite effects. Moreover, Ang-(1-7) augmented effects of Ang II in CHF rats. The effects of Ang-(1-7) were blocked by A-779, adenylyl cyclase inhibitor SQ22536, protein kinase A inhibitor Rp-cAMP, superoxide anion scavenger tempol and NAD(P)H oxidase inhibitor apocynin. Mas and AT1 receptor protein expressions, Ang-(1-7) and Ang II levels in CHF increased. Conclusions: These results indicate that Ang-(1-7) in paraventricular nucleus enhances CSAR and sympathetic output not only by exerting its own effects but also by augmenting the effects of Ang II through Mas receptor in CHF. Endogenous Ang-(1-7)/Mas receptor activity contributes to CSAR enhancement and sympathetic activation in CHF, and NAD(P)H oxidase-derived superoxide anions and the cAMP-PKA signaling pathway are involved in mediating the effects of Ang-(1-7) in CHF.
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