The existing terahertz detectors based on complementary metal oxide semiconductor cannot meet the design requirements of passive terahertz focal plane imaging chips owing to the problems of excessive noise or high-power consumption. To overcome this limitation, this study innovatively proposes using the gate of an N-type metal oxide semiconductor (NMOS) as a matching impedance of a multi-band terahertz on-chip antenna. In this way, the conversion of incident radiation into heat is achieved, and it is concentrated above the NMOS channel. The temperature characteristics of the equivalent impedance of the NMOS in the cutoff region are used to measure the incident radiated power without the DC bias current. The principle and simulation results of the proposed detector are given by system modeling, multi-band terahertz on-chip antenna design, and detector design. The experimental results show that the noise equivalent power of the proposed detector is very close to 1 pW/(Hz)^0.5 under liquid nitrogen cooling, which can meet the design requirements of passive terahertz focal plane imaging chips.

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Silicosis is an occupational lung disease that is common worldwide. In recent years, coronavirus disease 2019 (COVID-19) has provided daunting challenges to public healthcare systems globally. Although multiple studies have shown a close link between COVID-19 and other respiratory diseases, the inter-relational mechanisms between COVID-19 and silicosis remain unclear. This study aimed to explore the shared molecular mechanisms and drug targets of COVID-19 and silicosis. Gene expression profiling identified four modules that were most closely associated with both diseases. Furthermore, we performed functional analysis and constructed a protein–protein interaction network. Seven hub genes (budding uninhibited by benzimidazoles 1 [BUB1], protein regulator of cytokinesis 1 [PRC1], kinesin family member C1 [KIFC1], ribonucleotide reductase regulatory subunit M2 [RRM2], cyclin-dependent kinase inhibitor 3 [CDKN3], Cyclin B2 [CCNB2], and minichromosome maintenance complex component 6 [MCM6]) were involved in the interaction between COVID-19 and silicosis. We investigated how diverse microRNAs and transcription factors regulate these seven genes. Subsequently, the correlation between the hub genes and infiltrating immune cells was explored. Further in-depth analyses were performed based on single-cell transcriptomic data from COVID-19, and the expression of hub-shared genes was characterized and located in multiple cell clusters. Finally, molecular docking results reveal small molecular compounds that may improve COVID-19 and silicosis. The current study reveals the common pathogenesis of COVID-19 and silicosis, which may provide a novel reference for further research.