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Traditional centralized transactions require a control center for user demand matching, settlement and other processes. However, with the increase in the penetration rate of distributed energy in the community, the explosive increase in the number of transactions leads to a decrease in efficiency and it is difficult to guarantee user privacy and information security. The smart contract technology based on blockchain technology has the characteristics of decentralization, traceability and tamper resistance, and these key factors show unique advantages in distributed energy transactions. This paper explores Ethereum and smart contract technology, designs a peer-to-peer energy sharing mechanism with reward and punishment incentives and establishes a smart contract trading platform for smart community-based virtual power plant (CVPP). This paper verifies the functionality and effectiveness of smart contract. The results show that when the supply and demand ratio changes, the user can conduct energy transactions according to the contract without a third-party organization, which solves the problem of trust between the two parties and achieves the expected effect and runs successfully. In addition, the simulation results show that the peer-to-peer transaction based on smart contracts reduces the energy cost per household and increases the total benefit of CVPP.

Abstract Background Dysregulation of long non-coding RNAs has been implied to connect with cancer progression. This research was to decipher the mechanism of long non-coding RNA SDCBP2-AS1 in ovarian cancer (OC) through regulation of microRNA (miR)-100-5p and ependymin-related protein 1 (EPDR1). Methods LncRNA SDCBP2-AS1 and EPDR1 levels in OC were assessed by Gene Expression Profiling Interactive Analysis. lncRNA SDCBP2-AS1, miR-100-5p, and EPDR1 levels in OC tissues and cells were determined. SKOV3 and A2780 cells were transfected with lncRNA SDCBP2-AS1, miR-100-5p, and EPDR1-related plasmids or sequences, and then their functions in cell viability, apoptosis, migration, and invasion were evaluated. The interplay of lncRNA SDCBP2-AS1, miR-100-5p, and EPDR1 was clarified. Results LncRNA SDCBP2-AS1 and EPDR1 levels were suppressed whilst miR-100-5p level was elevated in OC. After upregulating lncRNA SDCBP2-AS1 or EPDR1, viability, migration, and invasion of OC cells were impaired, and apoptosis rate was increased. Downregulating EPDR1 or upregulating miR-100-5p partially mitigated upregulated lncRNA SDCBP2-AS1-induced impacts on the biological functions of OC cells. LncRNA SDCBP2-AS1 sponged miR-100-5p, and EPDR1 was targeted by miR-100-5p. Conclusion It is illustrated that lncRNA SDCBP2-AS1 regulates EPDR1 by sponge adsorption of miR-100-5p to inhibit the progression of OC.