Robust Control of a New Asymmetric Teleoperation Robot Based on a State Observer.

This study is mainly about the designation of a new type of haptic device and an asymmetric teleoperation robot system. Aiming at the problems of tracking and transparency of an asymmetric teleoperation system, a robust control algorithm based on a state observer was proposed. The Haptic Device was designed and was chosen as the master-robot of the system. The Baxter dual-arm robot was chosen as the slave-robot of the system. The simulation experiment of robust control based on a state observer of the asymmetric teleoperation robot was carried out. The experiment results showed that the maximum values of displacement tracking errors in three directions x, y, and z are 0.02 m, 0.01 m, and 0.015 m, respectively. Compared with single- joint PID control, the performance of the new control algorithm is improved. The force feedback experiment on the real asymmetric teleoperation robot system was carried out. The results showed that the force feedback wave is consistent with the actual situation and showed that the robust control algorithm proposed is superior to PID. Therefore, the algorithm perfectly satisfied the system. The experiment parameters also demonstrate that the haptic device satisfies the design requirements of the asymmetric teleoperation robots system and the industry standards.

Exendin-4 impairs the autophagic flux to induce apoptosis in pancreatic acinar AR42J cells by down-regulating LAMP-2.

This study aimed to explore the mechanism of impaired autophagy flux induced by exendin-4 and its role on cell apoptosis in pancreatic AR42J cells. The AR42J cells were treated with various concentration of exendin-4 for several time points to assess its cytotoxicity by MTT assay. Then the AR42J cells were treated by 10pM exendin-4 for 72 h, the cell death was analyzed by flow cytometry and caspase-3 level was examined by Western blot with or without the pretreatment of z-VAD-fmk to testify whether exendin-4 induces the cell apoptosis. The protein levels of LC3B, p62 and LAMP-2 were assessed by Western blot, the mRNA level of LAMP-2 was quantified by quantitative PCR in the absence or presence of LAMP-2 over-expression plasmid and the expression and activity of CatB and CatL were tested by ELISA or activity assay methods in AR42J cells treated by exendin-4. The normal rats and the diabetes-model rats by high-fat and high-sugar diet for two month then with streptozotocin intraperitoneally were subcutaneously injected with exendin-4 for 10 weeks to test the expression of LAMP-2 mRNA and protein in the pancreas. Cells pretreated with Bafilomycin A1 were detected for LC3B and p62 expressions by Western blot. Cells pretreated by 3-MA were used to assess whether 3-MA can protect from exendin-4 cytotoxicity. We found that exendin-4 can decrease the AR42J cell viability as well as increase the cell death and cleaved caspase-3 level, which all can be inhibited by z-VAD-fmk. Exendin-4 can downregulate the expression of LAMP-2 and then impair the autophagy flux to induce the accumulation of LC3B-II and p62, but cannot change the expression and activity of CatB and CatL. Bafilomycin A1 almostly have no impact on the change of LC3B and p62 protein levels induced by exendin-4. Both 3-MA and overexpressed LAMP-2 can reduce the cytotoxicity of exendin-4. Therefore, we considered the down-regulation of LAMP-2 which can impair the autophagy flux by inhibiting the fusion of autophagosomes with lysosomes to induce the AR42J cell apoptosis as the potential mechanism of chronic pancreatitis induced by exendin-4.