As the problem of light pollution becomes more serious, more and more scholars pay attention to this issue and carry out related research. In the perspective of cities, the measurements of light pollution mainly focus on the brightness of the sky or artificial lighting on the ground. However, there is lack of research on the whole urban space. With the two-dimensional brightness analyses, this paper processes the changes of the light environment of the whole urban space into image quantization. It gets the 3D and 2D light environment changes of luminance distribution, color temperature distribution and chromaticity in the three space layers, the ground layer, the urban canopy layer and the sky layer, from dusk with natural light to night with artificial lighting completely. It is found that the brightness difference between the light environments among the three city levels gradually reduces with the measuring time, and the final values maintain at 0.11~0.25 cd/m². In the ground layer, the light environment is mainly affected by the lighting facilities, and vegetation can prevent the light from scattering up. The light environment of the urban canopy layer is the brightest in the whole city space and has the largest influence on the sky layer. The color concentrates in the range of yellow and red. The color temperature near the ground distributes in 3000K~15000K, and near the sky distributes in 2300K~2700K which is warmer than the natural night sky. The sky brightness of Dalian city is about 951 times than the natural night sky.

(1) Background: Heart failure (HF) is the final stage of multiple cardiac diseases, which has now become a severe public health problem worldwide. β-Adrenergic receptor (β-AR) overactivation is a major pathological factor associated with multiple cardiac diseases and mediates cardiac fibrosis and inflammation. Previous study has demonstrated that Bruton's tyrosine kinase (BTK) mediated cardiac fibrosis by TGF-β related signal pathways, indicating that BTK was a potential drug target for cardiac fibrosis. Zanubrutinib, a second-generation BTK inhibitor, has shown anti-fibrosis effects in previous research. However, it is unclear whether Zanubrutinib can alleviate cardiac fibrosis induced by β-AR overactivation;(2) Methods: In vivo: Male C57BL/6J mice were treated with or without the β-AR agonist isoproterenol (ISO) to establish cardiac fibrosis animal model. Here, results showed that BTK inhibitor Zanubrutinib (ZB) had a great effect on cardiac fibrosis and inflammation induced by β-AR. In vitro: Results showed that ZB alleviated β-AR-induced cardiac fibroblast activation and macrophage proinflammatory cytokine production. Further mechanism studies demonstrated that ZB inhibited β-AR-induced cardiac fibrosis and inflammation by BTK、STAT3、NF-κB and PI3K/Akt signal pathways both in vivo and in vitro; (4) Conclusions: our research provides evidence that ZB ameliorates β-AR-induced cardiac fibrosis and inflammation.