The 3rd Generation Partnership Project (3GPP) recommends an accurate and compatible stochastic channel model for 0–100 GHz frequency band, which is useful to design, optimize, and evaluate the fifth‐generation (5G) systems. This standardized model can be acquired by generating the large‐ and small‐scale fading models. This article firstly reviews the main existing channel models suitable for millimeter‐wave (mmWave) frequency band as well as the typical channel modeling methods, i.e. the deterministic and stochastic models. Secondly, the generation procedure of stochastic channel model in the 3GPP standard (TR 38.901) is illustrated in detail. The large‐ and small‐scale fading parts are also simulated to demonstrate the effect of channel parameters on the channel characteristics. Finally, as an alternative model in the 3GPP standard, the map‐based hybrid channel model is demonstrated and analyzed. When the digital map and material parameters of obstacles are known, this model can predict the channel characteristics accurately using the ray‐tracing (RT) method.

Fibrosis contributes to graft loss in chronic renal allograft injury. Endothelial‐to‐mesenchymal transition (EndMT) plays an important role in the development of fibrosis following kidney transplantation. Autophagy plays an important role in the homeostasis of diverse cell types including endothelial cells. Here we demonstrate that inhibition of autophagy by treatment with 3-methyladenine (3-MA) or by silencing autophagy-related (ATG)5 promoted interleukin (IL)-6–dependent EndMT in human umbilical vein endothelial cells (HUVECs) and human renal glomerular endothelial cells (HRGECs), and autophagy inactivation was associated with EndMT in patients with chronic allograft dysfunction. IL-6 level was significantly higher in the culture medium of HUVECs transfected with ATG5 siRNA or treated with 3-MA compared to the respective control groups. IL-6 application induced EndMT in HUVECs and HRGECs, whereas antibody-mediated neutralization of IL-6 suppressed EndMT induced by ATG5 silencing. The protective role of curcumin (Cur) against allograft fibrosis was confirmed in a rat kidney transplantation model of F344 donors to Lewis recipients. Curcumin—a natural polyphenol compound with known antifibrotic effects in various tissues—alleviated IL-6–induced EndMT and promoted autophagy in the allografted organ and in HUVECs. This is the first demonstration of the role of autophagy in renal allograft fibrosis; our findings indicate that curcumin can alleviate chronic renal allograft injury by suppressing IL-6–dependent EndMT via activation of autophagy.

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