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Articles by Meihong Liu
Total Records ( 2 ) for Meihong Liu
  Wei Li , Meihong Liu , Deren Gong and Dengping Duan
  A Huber-based Kalman Filter (HKF) is presented to non-Gaussian random measurement errors. The measurement noise uncertainty is tackled at each filter step by minimizing a criterion function that is original from Huber technique. A recursive algorithm is also provided to solve the criterion function. The proposed HKF algorithm has been tested in attitude estimation using gyroscope and star tracker sensors for a single spacecraft in flight simulations. Simulation results demonstrate the superior performance of the proposed filter as compared to the standard Kalman Filter (KF) in the presence of non-Gaussian measurement noise.
  Meihong Liu , Liangpeng Yang , Ling Zhang , Baoying Liu , Randall Merling , Zheng Xia and Chou- Zen Giam
  Infection by the human T-cell leukemia virus type 1 (HTLV-1) is thought to cause dysregulated T-cell proliferation, which in turn leads to adult T-cell leukemia/lymphoma. Early cellular changes after HTLV-1 infection have been difficult to study due to the poorly infectious nature of HTLV-1 and the need for cell-to-cell contact for HTLV-1 transmission. Using a series of reporter systems, we show that HeLa cells cease proliferation within one or two division cycles after infection by HTLV-1 or transduction of the HTLV-1 tax gene. HTLV-1-infected HeLa cells, like their tax-transduced counterparts, expressed high levels of p21CIP1/WAF1 and p27KIP1, developed mitotic abnormalities, and became arrested in G1 in senescence. In contrast, cells of a human osteosarcoma lineage (HOS) continued to divide after HTLV-1 infection or Tax expression, albeit at a reduced growth rate and with mitotic aberrations. Unique to HOS cells is the dramatic reduction of p21CIP1/WAF1 and p27KIP1 expression, which is in part associated with the constitutive activation of the phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) pathway. The loss of p21CIP1/WAF1 and p27KIP1 in HOS cells apparently allows HTLV-1- and Tax-induced G1 arrest to be bypassed. Finally, HTLV-1 infection and Tax expression also cause human SupT1 T cells to arrest in the G1 phase of the cell cycle. These results suggest that productive HTLV-1 infection ordinarily leads to Tax-mediated G1 arrest. However, T cells containing somatic mutations that inactivate p21CIP1/WAF1 and p27KIP1 may continue to proliferate after HTLV-1 infection and Tax expression. These infected cells can expand clonally, accumulate additional chromosomal abnormalities, and progress to cancer.
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