Metasurfaces have been extensively studied for generating electromagnetic waves carrying orbital angular momentum (OAM). In particular, programmable metasurfaces enable real‐time switching between multiple OAM modes in a digital manner. However, the current programmable metasurfaces are mostly based on reflective mode, which suffer from low efficiency as well as serious feed blockage. In this paper, a transmissive programmable metasurface is presented for the highly efficient generation of multimode convergent OAM beams. The proposed transmissive metasurface is composed of electronically reconfigurable units with 1‐bit phase resolution (0/π), which are obtained by integrating two PIN diodes in the radiating layer for current direction modulation. Through the antisymmetry configuration of the two PIN diodes, nearly uniform transmission magnitudes but inversed phase states in a wide band can be obtained. The simulation results show that the proposed reconfigurable unit can achieve good 1‐bit phase tuning, with minimum insertion loss of 0.2 dB and 2 dB transmission bandwidth of more than 10%. Through the dynamic modulation of the quantized code distributions on the metasurface, programmable multimode OAM beams can thus be constructed. Both simulated and measured results verify the effectiveness of the proposed design.

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IntroductionProstate cancer is the most common noncutaneous cancer and the second leading cause of cancer-related mortality worldwide and the third in USA in 2017. Chelerythrine (CHE), a naturalbenzo[c]phenanthridine alkaloid, formerly identified as a protein kinase C inhibitor, has also shown anticancer effect through a number of mechanisms. Herein, effect and mechanism of the CHE-induced apoptosis via reactive oxygen species (ROS)-mediated endoplasmic reticulum (ER) stress in prostate cancer cells were studied for the first time.MethodsIn our present study, we investigated whether CHE induced cell viability decrease, colony formation inhibition, and apoptosis in a dose-dependent manner in PC-3 cells. In addition, we showed that CHE increases intracellular ROS and leads to ROS-dependent ER stress and cell apoptosis.ResultsPre-treatment with N-acetyl cysteine, an ROS scavenger, totally reversed the CHE-induced cancer cell apoptosis as well as ER stress activation, suggesting that the ROS generation was responsible for the anticancer effects of CHE.ConclusionTaken together, our findings support one of the anticancer mechanisms by which CHE increased ROS accumulation in prostate cancer cells, thereby leading to ER stress and caused intrinsic apoptotic signaling. The study reveals that CHE could be a potential candidate for application in the treatment of prostate cancer.