We develop a compact full-color augmented reality near-eye display system with a multicolor holographic optical combiner and a freeform relay system. The digital image is produced by a full-color micro organic light-emitting diode (Micro-OLED) display module. The freeform relay system includes four freeform optics and a holographic optical mirror, which are employed to correct both the monochromatic and chromatic aberrations caused by the holographic optical combiner. The two multicolor holographic mirrors have a three-layer laminated structure and are delicately fabricated to yield an improved diffractive efficiency and a reduced efficiency difference for red, green, and blue colors. The high degrees of freedom of freeform optics, and the thin and light nature of the holographic optical combiner yield a compact form factor near-eye display system with a diagonal field of view (FOV) of 20° and the eye-box of 5 mm × 5 mm. Two prototypes are built to demonstrate the feasibility of the proposed display system.

Previous studies have reported that visfatin can regulate macrophage polarisation, which has been demonstrated to participate in cardiac remodelling. The aims of this study were to investigate whether visfatin participates in transverse aortic constriction (TAC)‐induced cardiac remodelling by regulating macrophage polarisation. First, TAC surgery and angiotensin II (Ang II) infusion were used to establish a mouse cardiac remodelling model, visfatin expression was measured, and the results showed that TAC surgery or Ang II infusion increased visfatin expression in the serum and heart in mice, and phenylephrine or hydrogen peroxide promoted the release of visfatin from macrophages in vitro. All these effects were dose‐dependently reduced by superoxide dismutase. Second, visfatin was administered to TAC mice to observe the effects of visfatin on cardiac remodelling. We found that visfatin increased the cross‐sectional area of cardiomyocytes, aggravated cardiac fibrosis, exacerbated cardiac dysfunction, further regulated macrophage polarisation and aggravated oxidative stress in TAC mice. Finally, macrophages were depleted in TAC mice to investigate whether macrophages mediate the regulatory effect of visfatin on cardiac remodelling, and the results showed that the aggravating effects of visfatin on oxidative stress and cardiac remodelling were abrogated. Our study suggests that visfatin enhances cardiac remodelling by promoting macrophage polarisation and enhancing oxidative stress. Visfatin may be a potential target for the prevention and treatment of clinical cardiac remodelling.