Autonomous motion and control of lower limb exoskeleton rehabilitation robot

Introduction: The lower limb exoskeleton rehabilitation robot should perform gait planning based on the patient’s motor intention and training status and provide multimodal and robust control schemes in the control strategy to enhance patient participation.Methods: This paper proposes an adaptive particle swarm optimization admittance control algorithm (APSOAC), which adaptively optimizes the weights and learning factors of the PSO algorithm to avoid the problem of particle swarm falling into local optimal points. The proposed improved adaptive particle swarm algorithm adjusts the stiffness and damping parameters of the admittance control online to reduce the interaction force between the patient and the robot and adaptively plans the patient’s desired gait profile. In addition, this study proposes a dual RBF neural network adaptive sliding mode controller (DRNNASMC) to track the gait profile, compensate for frictional forces and external perturbations generated in the human-robot interaction using the RBF network, calculate the required moments for each joint motor based on the lower limb exoskeleton dynamics model, and perform stability analysis based on the Lyapunov theory.Results and discussion: Finally, the efficiency of the APSOAC and DRNNASMC algorithms is demonstrated by active and passive walking experiments with three healthy subjects, respectively

Mitochondrial IRG1 traps MCL-1 to induce hepatocyte apoptosis and promote carcinogenesis

Abstract Hepatocarcinogenesis is initiated by repeated hepatocyte death and liver damage, and the underlying mechanisms mediating cell death and the subsequent carcinogenesis remain to be fully investigated. Immunoresponsive gene 1 (IRG1) and its enzymatic metabolite itaconate are known to suppress inflammation in myeloid cells, and its expression in liver parenchymal hepatocytes is currently determined. However, the potential roles of IRG1 in hepatocarcinogenesis are still unknown. Here, using the diethylnitrosamine (DEN)-induced hepatocarcinogenesis mouse model, we found that IRG1 expression in hepatocytes was markedly induced upon DEN administration. The DEN-induced IRG1 was then determined to promote the intrinsic mitochondrial apoptosis of hepatocytes and liver damage, thus enhancing the subsequent hepatocarcinogenesis. Mechanistically, the mitochondrial IRG1 could associate and trap anti-apoptotic MCL-1 to inhibit the interaction between MCL-1 and pro-apoptotic Bim, thus promoting Bim activation and downstream Bax mitochondrial translocation, and then releasing cytochrome c and initiating apoptosis. Thus, the inducible mitochondrial IRG1 promotes hepatocyte apoptosis and the following hepatocarcinogenesis, which provides mechanistic insight and a potential target for preventing liver injury and HCC