A broad range of dynamic metasurfaces has been developed for manipulating the intensity, phase and wavefront of electromagnetic radiation from microwaves to optical frequencies. However, most of these metasurfaces operate in single-input–output state. Here, we experimentally demonstrate a reconfigurable MEMS Fano resonant metasurface possessing multiple-input–output (MIO) states that performs logic operations with two independently controlled electrical inputs and an optical readout at terahertz frequencies. The far-field behaviour of Fano resonance exhibits XOR and XNOR operations, while the near-field resonant confinement enables the NAND operation. The MIO configuration resembling hysteresis-type closed-loop behaviour is realized through inducing electromechanically tuneable out-of-plane anisotropy in the near-field coupling of constituent resonator structures. The XOR metamaterial gate possesses potential applications in cryptographically secured terahertz wireless communication networks. Furthermore, the MIO features could lay the foundation for the realization of programmable and randomly accessible metamaterials with enhanced electro-optical performance across terahertz, infrared and optical frequencies.

Angiotensin-converting enzyme 2 (ACE2) is a newly discovered homolog of ACE whose actions oppose those of angiotensin II (AngII). However, the underlying mechanisms by which ACE2 effectively suppresses early atherosclerotic lesions remain poorly understood. Here, we show, both in vitro and in vivo, that ACE2 inhibited the development of early atherosclerotic lesions by suppressing the growth of vascular smooth muscle cells (VSMCs) and improving endothelial function. In a relatively large cohort animal study (66 rabbits), aortic segments transfected by Ad-ACE2 showed significantly attenuated fatty streak formation, neointimal macrophage infiltration, and alleviation of impaired endothelial function. Segments also showed decreased expression of monocyte chemoattractant protein 1, lectin-like oxidized low-density lipoprotein receptor 1, and proliferating cell nuclear antigen, which led to the delayed onset of atherosclerotic lesions. At the cellular level, ACE2 significantly modulated AngII-induced growth and migration in human umbilical vein endothelial cells and VSMCs. The antiatherosclerotic effect of ACE2 involved down-regulation of the ERKp38, JAK-STAT, and AngII-ROS-NF-κB signaling pathways and upregulation of the PI3K-Akt pathway. These findings revealed the molecular mechanisms of the antiatherosclerotic activity of ACE2 and suggested that modulation of ACE2 could offer a therapeutic option for treating atherosclerosis.atherosclerosis | endothelial cell | gene therapy | smooth muscle cell | signaling pathway A ccumulating evidence indicates that endothelial cell (EC) dysfunction and the proliferation and migration of vascular smooth muscle cells (VSMCs) are salient features of early atherosclerotic lesions, and that the renin-angiotensin system (RAS) plays an important role in the pathogenesis of atherosclerosis (1, 2). Angiotensin II (AngII) promotes EC dysfunction and VSMC proliferation and migration by increasing the expression of monocyte chemoattractant protein 1 (MCP-1) and lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1), leading to aggravation of atherosclerotic lesions (3-5). Delivery of ACE inhibitors or AngII type 1 receptor (AT 1 R) blockers to limit AngII bioactivity is an effective approach against atherosclerosis.Recent studies show that endogenous levels of AngII are regulated by the opposing action of two carboxypeptidases, angiotensin-converting enzyme (ACE) and angiotensin-converting enzyme 2 (ACE2). The latter is thought to counterbalance ACE by cleaving AngI into the inactive angiotensin 1-9 and cleaving AngII into the vasodilating and antiproliferative angiotensin 1-7 [Ang(1-7)]. ACE2 is thus considered a potential therapeutic target of RAS for the treatment of cardiovascular diseases by virtue of its key role in the formation of vasoprotective peptides from AngII (6-8). Our recent study using a rabbit atherosclerosis model showed that ACE2 overexpression stabilized aortic plaques at a late stage and attenuated the progression of early atherosclerotic lesions. These ther...

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