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  • Author: An-qi Li x
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Duo Qi, Jinfu Feng, An Liu, Junhua Hu, Hu Xu, Yongli Li and Muhammad Aqeel Ashraf


Learning from the motion principle of quadrotor, a symmetric propeller AUV, which has small size and low velocity is designed. Compared with the AUV equipped with rudders, it has better maneuverability and manipulation at low velocity. According to the Newton-Euler method, the 6 DOF kinematic model and dynamic model of the propeller AUV are established. A stability controller that consists of 3 different PID controllers is designed. It makes the depth and attitude angle as trigger conditions, and the relevant controller is chosen in different moving process. The simulation experiments simulate ideal motion state and disturbed motion state, and experiments results show that the stability controller based on combined sections method can make the best of mature technology of PID, and meet the control requirements in different stages. It has a higher respond speed and accuracy, improving the stability of the propeller AUV under the disturbance of complex ocean currents.

Open access

Tie-long Zheng, Ping-an Wang, Dian-li Wang, Cheng-fu Sun, Yuan Hong, Qi Wang and Jun Cheng


Objective To observe the biological function of human 3-hydroxyisobutyrate dehydrogenase (HIBADH).

Methods Human 3-hydroxyisobutyrate dehydrogenase (HIBADH, 3-hydroxy-2-methyl propanoate: NAD+ oxidoreductase) recombinant protein was expressed in E. coli BL21, and purified by Ni+ column. The special antisera was obtained from rabbits immunized by this purified antigen. On the distribution of HIBADH, it was found that HIBADH over-expressed in the injured liver cells when serious hepatitis occurred. The phenomenon was confirmed in the animal models of SD rats with acute liver cell injury induced by CCl4, but this phenomenon did not exist in the models induced by endotoxin combined with galactosamine. Further more, HIBADH’s overexpression in liver cells will induce cell necrosis through the pathway of oxidative stress.

Results When the liver cells injured by drug or other chemical materials, HIBADH will be compensationally over-expressed for the deficiency of energy, so liver cells can make enough ATP through brand-chain amino acid catabolism. However, the overexpression of HIBADH will be harmful for liver cells through the product of much more active oxygens which will induce the cell necrosis.

Conclusions HIBADH over-expression is a signal of the liver cell metabolism injury, and it can aggravate the liver cell injury through oxidative stress.