Fuzzy adaptive PID speed controller design for modern elevator traction machine

With the development of the times, elevator has become an essential transportation in our life. In order to meet the comfort of elevator operation, this paper investigates the design of the speed control system of elevator permanent magnet synchronous traction motor in combination with the elevator operation curve. The whole system is based on SVPWM and uses direct torque control combined with fuzzy adaptive PID to achieve accurate control of motor running speed. It includes the input signal module, control module, drive module and feedback module. Firstly, the analysis of each module in the system is completed, and the connection between the modules is established, as well as the control system. Then case studies are carried out on MATLAB/SIMULINK, and the actual running speed curve of the elevator is obtained, and the simulation results are analyzed to verify the stability and reliability of this speed control system and complete the design

Inhibition of TRPC6 degradation suppresses ischemic brain damage in rats

Brain injury after focal cerebral ischemia, the most common cause of stroke, develops from a series of pathological processes, including excitotoxicity, inflammation, and apoptosis. While NMDA receptors have been implicated in excitotoxicity, attempts to prevent ischemic brain damage by blocking NMDA receptors have been disappointing. Disruption of neuroprotective pathways may be another avenue responsible for ischemic damage, and thus preservation of neuronal survival may be important for prevention of ischemic brain injury. Here, we report that suppression of proteolytic degradation of transient receptor potential canonical 6 (TRPC6) prevented ischemic neuronal cell death in a rat model of stroke. The TRPC6 protein level in neurons was greatly reduced in ischemia via NMDA receptor–dependent calpain proteolysis of the N-terminal domain of TRPC6 at Lys16. This downregulation was specific for TRPC6 and preceded neuronal death. In a rat model of ischemia, activating TRPC6 prevented neuronal death, while blocking TRPC6 increased sensitivity to ischemia. A fusion peptide derived from the calpain cleavage site in TRPC6 inhibited degradation of TRPC6, reduced infarct size, and improved behavioral performance measures via the cAMP response element–binding protein (CREB) signaling pathway. Thus, TRPC6 proteolysis contributed to ischemic neuronal cell death, and suppression of its degradation preserved neuronal survival and prevented ischemic brain damage