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The current wind silk-feeding system in cigarette factories has defects such as randomness, uncertainty, and frequent changes in wind volume, which are the fundamental causes of the system’s non-energy saving and unstable silk-feeding wind speed. This paper proposes to construct a new wind silk feeding system based on fuzzy RBF by utilizing the functional equivalence of fuzzy inference systems and RBF neural networks from a global perspective. Then, according to the process characteristics of the wind balance control system, the use of fuzzy networks for PID control of the core system is proposed. The practical application of the new wind power silk feeding system confirms the energy-saving effect of the improved program. Measurement results show that after the improvement of the fan frequency from 50Hz down to 38Hz, power from 35kW down to 25kW, the system runs smoothly, the wind speed is stable, and the energy saving can be up to 25%~40%. This paper not only provides a new way of thinking for the optimal design of wind power wire feeding projects but also has reference value for guiding the selection and control scheme of the project.

Muscarinic acetylcholine receptors (MRs) play important roles in the regulation of hepatic fibrosis and the receptor agonists and antagonists can affect hepatocyte proliferation. However, little is known about the impact of M 3R subtypes and associated signaling pathways on liver injury. The aim of this study is to explore the function and mechanism of M 3R in the regulation of liver injury. We evaluate liver injury and detect the changes in related indexes, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), hydroxyproline (HYP), and transforming growth factor-β1 (TGF-β1), after administration of an M 3R agonist. Western blot analysis and qRT-PCR show that the transcription factor Sp1 and long noncoding RNA (lncRNA) Gm2199 are also changed significantly. Rescue assay is performed to further confirm that M 3R contributes to the progression of hepatocyte proliferation through regulating Sp1 and Gm2199. The activated M 3R can specifically regulate Gm2199 by inhibiting the expression of Sp1. Meanwhile, Gm2199 directly regulates miR-212, and ERK is a potential target of miR-212. Collectively, these findings define a novel mechanism for activating M 3R to reverse liver injury, which affects hepatocyte proliferation through the Sp1/Gm 2199/miR-212/ERK axis.