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Articles by Jie Ma
Total Records ( 2 ) for Jie Ma
  Jing Liu , Jie Ma , Jin-wen Tian , Zhi-wei Kang and Paul White
  In order to reduce the impact of the pulsar direction error on the navigation system performance, a novel X-ray pulsar navigation technique is proposed. Through analyzing the system bias caused by the pulsar direction error, it can be seen that the system bias is slowly time-varying. Based on the analysis result, the augmented state unscented Kalman filter (ASUKF), in which the system bias is treated as the augmented state, is designed here to deal with the system bias and estimate spacecraft’s positions and velocities. The simulation results demonstrate the effectiveness and robustness of the proposed navigation method. The ASUKF-based navigation method for spacecraft is more accurate than the method based on unscented Kalman filter (UKF) in the presence of the pulsar direction error.
  Ingyu Kim , Cunxi Li , Dan Liang , Xing-Zhen Chen , Robert J. Coffy , Jie Ma , Ping Zhao and Guanqing Wu
  Autosomal dominant (ADPKD) and autosomal recessive (ARPKD) polycystic kidney disease are caused by mutations in Pkd1/Pkd2 and Pkhd1, which encode polycystins (PCs) and fibrocystin/polyductin (FPC). Our recent study reported that a deficiency in FPC increases the severity of cystic disease in Pkd2 mutants and down-regulates PC2 in vivo, but the precise molecular mechanism of these effects is unknown (Kim, I., Fu, Y., Hui, K., Moeckel, G., Mai, W., Li, C., Liang, D., Zhao, P., Ma, J., Chen, X.-Z., George, A. L., Jr., Coffey, R. J., Feng, Z. P., and Wu, G. (2008) J. Am. Soc. Nephrol. 19, 455–468). In this study, through the use of deletion and mutagenesis strategies, we identified a PC2-binding domain in the intracellular C terminus of FPC and an FPC-binding domain in the intracellular N terminus of PC2. These binding domains provide a molecular basis for the physical interaction between PC2 and FPC. In addition, we also found that physical interaction between the binding domains of PC2 and FPC is able to prevent down-regulation of PC2 induced by loss of FPC. In vivo, we generated a mouse model of ADPKD with hypomorphic Pkd2 alleles (Pkd2nf3/nf3) and show that PC2 down-regulation is accompanied by a phenotype similar to that of Pkhd1–/– mice. These findings demonstrate a common mechanism underlying cystogenesis in ADPKD and ARPKD and provide insight into the molecular relationship between PC2 and FPC.
 
 
 
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