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Träfflista för sökning "WFRF:(Zhang Ning) srt2:(2000-2004)"

Sökning: WFRF:(Zhang Ning) > (2000-2004)

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  • Ben Slimane, Slimane, et al. (författare)
  • On the Capacity of CDMA with Linear Successive Interference Cancellation
  • 2003
  • Ingår i: European transactions on telecommunications. - : Wiley. - 1124-318X .- 2161-3915 .- 1541-8251. ; 14:6, s. 501-513
  • Tidskriftsartikel (refereegranskat)abstract
    • Combined power control and interference cancellation in CDMA systems can be a very efficient resourcemanagement tool. While conventional power control tries to maintain equal received power or balancedsignal-to-interference ratio (SIR), successive interference cancellation (SIC) in multi-user detection (MUD)relies more on the disparities between the powers of the different users. The combination can save morepower into the system and thus a room for a better capacity. This paper investigates the interaction between power control and linear SIC in a single-rate CDMAsystem and its impact on the system capacity. The obtained results show that interference cancellation canimprove the capacity of CDMA and relax power control requirements. The full integration of power controland linear SIC detection is shown to provide excellent resource management in CDMA systems. Limitedinterference cancellation can be a good solution for CDMA systems as it provides considerable capacitygain with reduced complexity. An upper bound on the system capacity as a function of the cancellationparameters used along the different stages of the SIC detector is derived. Investigation of the optimumdecoding order is also provided in this paper.
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4.
  • Cai, Meng, et al. (författare)
  • On the Capacity of CDMA with Linear Successive Interference Cancellation
  • 2003
  • Ingår i: European Transactions on Telecommunications. - New York : IEEE. - 0852967535 ; , s. 362-366
  • Konferensbidrag (refereegranskat)abstract
    • Combined power control and interference cancellation in CDMA systems can be a very efficient resource management tool. While conventional power control tries to maintain equal received power or balanced SIR, Successive Interference Cancellation (SIC) in Multi-User Detection (MUD) relies more on the disparities between the powers of the different users. The combination can save more power into the system and thus a room for better capacity. This paper investigates the interaction between power control and linear SIC in a single rate CDMA system and its impact on the system capacity. The obtained results show that interference cancellation can improve the capacity of CDMA and relax power control requirements. The full integration of power control and SIC is shown to provide excellent resource management in CDMA systems. Limited cancellation can be a good solution for CDMA systems as it provides considerable capacity gain with reduced complexity. An upper bound on the system capacity as a function of the number of canceled signals is derived. Investigation of the optimum decoding order is also provided in this paper.
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5.
  • Luo, Guanghua, et al. (författare)
  • Apolipoprotein M
  • 2004
  • Ingår i: Lipids in Health and Disease. - 1476-511X. ; 3
  • Forskningsöversikt (refereegranskat)abstract
    • Apolipoprotein M (apoM) is a 26-kDa protein that is mainly associated with high-density lipoprotein (HDL) in human plasma, with a small proportion present in triglyceride-rich lipoproteins (TGRLP) and low-density lipoproteins (LDL). Human apoM gene is located in p21.31 on chromosome 6 (chromosome 17, in mouse). Human apoM cDNA (734 base pairs) encodes 188-amino acid residue-long protein. It belongs to lipocalin protein superfamily. Human tissue expression array study indicates that apoM is only expressed in liver and in kidney and small amounts are found in fetal liver and kidney. In situ apoM mRNA hybridization demonstrates that apoM is exclusively expressed in the hepatocytes and in the tubule epithelial cells in kidney. Expression of apoM could be regulated by platelet activating factor (PAF), transforming growth factors (TGF), insulin-like growth factor (IGF) and leptin in vivo and/or in vitro. It has been demonstrated that apoM expression is dramatically decreased in apoA-I deficient mouse. Hepatocyte nuclear factor-1alpha (HNF-1alpha) is an activator of apoM gene promoter. Deficiency of HNF-1alpha mouse shows lack of apoM expression. Mutations in HNF-1alpha (MODY3) have reduced serum apoM levels. Expression of apoM is significantly decreased in leptin deficient (ob/ob) mouse or leptin receptor deficient (db/db) mouse. ApoM concentration in plasma is positively correlated to leptin level in obese subjects. These may suggest that apoM is related to the initiation and progression of MODY3 and/or obesity.
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6.
  • Xu, Ning, et al. (författare)
  • Effects of platelet-activating factor, tumor necrosis factor, and interleukin-1alpha on the expression of apolipoprotein M in HepG2 cells.
  • 2002
  • Ingår i: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 292:4, s. 944-950
  • Tidskriftsartikel (refereegranskat)abstract
    • Apolipoprotein M (apoM) is a recently discovered human apolipoprotein predominantly present in high-density lipoprotein (HDL) in plasma, exclusively expressed in liver and in kidney. The function of apoM is yet unknown. The human apoM gene is located in the major histocompatibility complex class III region on chromosome 6. Because many genes located in this region are related to the immune response, we have investigated whether apoM might also be involved in the host inflammatory response. In this study we examined effects of the platelet-activating factor (PAF), tumor necrosis factor (TNF-alpha), and interleukin-1alpha (IL-1alpha) on apoM expression in a hepatoblastoma cell line, HepG2 cells. PAF significantly enhanced the apoM mRNA levels and the secretion of apoM in HepG2 cell cultures. The enhancement of apoM secretion is seen at a low concentration of PAF (2 ng/ml), whereas a high concentration of PAF increases both the apoM mRNA levels and apoM secretion. Neither TNF-alpha nor IL-1alpha influenced apoM mRNA level and secretion. Furthermore, Lexipafant, a PAF-receptor (PAF-R) antagonist significantly suppressed the mRNA level and the secretion of apoM in HepG2 cells in a dose-dependent manner. Neither PAF nor Lexipafant influenced the mRNA levels and the secretion of apoA-I, apoB and apoE in HepG2 cells, indicating that the effects of PAF or Lexipafant on the apoM production on hepatic cells are selective for apoM. The cellular mechanism of the effects of PAF or Lexipafant on apoM metabolism requires further investigations.
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7.
  • Xu, Ning, et al. (författare)
  • Transforming growth factor-beta down-regulates apolipoprotein M in HepG2 cells.
  • 2004
  • Ingår i: Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids. - : Elsevier BV. - 1388-1981. ; 1683:1-3, s. 33-37
  • Tidskriftsartikel (refereegranskat)abstract
    • Apolipoprotein M (apoM) is a novel apolipoprotein presented mostly in high-density lipoprotein (HDL) in human plasma, and is exclusively expressed in liver and in kidney. The pathophysiological function of apoM has not yet been elucidated. Apolipoprotein B (apoB), the characteristic apolipoprotein of low-density lipoprotein (LDL), is like apoM, a very hydrophobic protein, and thereafter they both must co-circulate with lipoprotein particles in plasma. The cytokine, transforming growth factor-beta (TGF-beta), has been shown to decreased apoB secretion in HepG2 cells, and we hypothesized that TGF-beta may have the same effects on apoM expression in HepG2 cells. In the present study, we used real-time RT-PCR to analyze apoM and apoB mRNA levels during administration of TGF-beta, as well as TGF-alpha, epidermal growth factor (EGF) and hepatic growth factor (HGF). TGF-beta significantly inhibited both apoM and apoB mRNA expression in HepG2 cells. The inhibitory effects of TGF-beta were dose-dependent, i.e. 1 ng/ml of TGF-beta decreased apoM mRNA levels by 30%, and 10 or 100 ng/ ml of TGF-beta decreased apoM mRNA levels more than 65%. The effect of TGF-beta on apoB mRNA expression was slightly weaker than that of apoM, with a maximum effect at 10 or 100 ng/ml TGF-beta where apoB mRNA levels decreased about 55%. The inhibitory effects of TGF-beta on apoM and apoB mRNA levels also increased with increasing incubation time, where the maximum effect was obtained at 24 h. Moreover TGF-alpha, EGF and HGF all decreased both apoM and apoB mRNA levels, but to a less extent than TGF-beta. Further, all four cytokines had more pronounced effects on apoM mRNA expression than apoB mRNA expression. The present study suggested that apoM, like apoB, may be involved in the hepatic lipoprotein assembly in vivo. (C) 2004 Elsevier B.V. All rights reserved.
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8.
  • Zhang, XY, et al. (författare)
  • Expression pattern of apolipoprotein M during mouse and human embryogenesis
  • 2004
  • Ingår i: Acta Histochemica. - : Elsevier BV. - 0065-1281. ; 106:2, s. 123-128
  • Tidskriftsartikel (refereegranskat)abstract
    • Apolipoprotein M (apoM) is a recently discovered human apolipoprotein predominantly present in high-density lipoprotein (HDL), and in minor proportions in triglyceride-rich lipoprotein (TGRLP) and low-density lipoprotein (LDL). The gene encoding apoM is present in all mammalian genomes. The identity of the apoM gene of human, rat and mouse is over 80%. However, the (patho)physiological functions of apoM are unknown yet. In the present study, we investigated apoM expression patterns during mouse and human embryogenesis. ApoM transcripts were detectable in mouse embryos from day 7.5 to day 18.5. ApoM was expressed at low levels at day 7.5, its expression increased significantly at day 9.7, decreased at day 10.5, and then increased continually up to day 18.5. ApoM-positive cells appeared mainly in liver of day-12 embryos as detected by in situ hybridization. In day-15 embryos, apoM was expressed in both liver and kidney. During human embryogenesis, apoM was mainly expressed in liver and kidney and little was found in small intestine as determined by mRNA array of human fetal. normal tissues. ApoM was also detected in stomach and skeletal muscle in early stages of embryogenesis (3-5 months). (C) 2004 Elsevier GmbH. All rights reserved.
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9.
  • Zhang, XY, et al. (författare)
  • Specific tissue expression and cellular localization of human apolipoprotein M as determined by in situ hybridization
  • 2003
  • Ingår i: Acta Histochemica. - : Elsevier BV. - 0065-1281. ; 105:1, s. 67-72
  • Tidskriftsartikel (refereegranskat)abstract
    • Apolipoprotein M (apoM) is a recently discovered human apolipoprotein predominantly present in high-density lipoprotein (HDL), and in minor proportion in triglyceride-rich lipoprotein (TGRLP) and low-density lipoprotein (LDL). The gene coding for apoM has been detected in all mammal genomes. The function of apoM is unknown yet. In the present study, we demonstrated that apoM is exclusively expressed in a strong manner in adult liver and kidney, and is expressed weakly in fetal liver and kidney as detected with human multiple tissue expression array. Both immumohistochemical staining and apoM mRNA in situ hybridization demonstrated that apoM was exclusively expressed in hepatocytes in human liver and in tubular epithelial cells in human kidney. The present study helps to elucidate the pathophysiological functions of apoM in vivo.
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