PubMed · 10096285
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R W Wagner, D Lipovsek. 1999. Smartbombs and cloaking devices.. https://doi.org/10.1038/6966
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The persistence of wheezing after early wheezing episodes in infancy may be related to the virus involved and to the type of inflammation during the initial wheezing. The role of mast cell activation and leukotriene secretion in wheezing, and the relation to outcome, is not known. Our objective was to study markers of mast cell activation and leukotriene secretion from wheezing infants, and the relation to respiratory syncytial virus (RSV) infection and persistent wheezing. Urinary 9alpha,11beta-PGF(2), a marker of mast cell activation, and urinary leukotriene E4 were measured in 106 infants hospitalized for wheezing during their first year of life. Results were related to the presence of RSV infection and the persistence of wheezing at follow-up 20 months later. Levels of 9alpha,11beta-PGF(2) were higher in infants positive for RSV than in those with RSV negative wheezing, but both groups had higher levels than controls. Leukotriene E4 levels were higher in wheezing infants than in controls. Urinary 9alpha,11beta-PGF(2) levels were higher in infants with transient compared with persistent wheezing. We found a positive correlation between 9alpha,11beta-PGF(2) and leukotriene E4, strongest in infants with RSV negative disease and in infants with persistent wheezing. The results suggest that mast cells play an important role in infant wheezing, and may be a major source of leukotriene secretion in these infants. Mast cell activation and leukotriene secretion were not associated with persistent wheezing.
AIM: To study the effect of a novel targeted ribonuclease (TN), the fusion protein of HBVc and human eosinophil-derived neurotoxin (hEDN), on the HBV replication in vitro. METHODS: The gene encoding the targeted ribonuclease was cloned into pcDNA3.1 (-) to form recombinant eukaryotic expression vector p/TN. Control plasmids, including p/hEDN, p/HBVc, and p/TNmut in which a Lys113-Arg mutation was introduced by sequential PCR to eliminate the ribonuclease activity of hEDN, were also constructed. Liposome-mediated transfection of 2.2.15 cells by p/TN, p/TNmut, p/hEDN, p/HBVc, and pcDNA3.1 (-), or mock transfection was performed. After that, RT-PCR was used to verify the transgene expression. Morphology of the transfected cells was observed and MTT assay was performed to detect the cytotoxicity of transgene expression. Concentration of HBsAg in the supernatant of the transfected cells was measured using solid-phase radioimmunoassay. RESULTS: Transgenes were successfully expressed in 2.2.15 cells. No obvious cytotoxic effect of transgene expression on 2.2.15 cells was found. The HBsAg concentration in the p/TN transfected cells was reduced by 58 % compared with that of mock transfected cells. No such an effect was found in all other controls. CONCLUSION: The targeted ribonuclease can inhibit HBV replication in vitro while it has no cytotoxicity on host cells. The targeted ribonuclease may be used as a novel antiviral agent for human HBV infection.
AIM: To construct Tat-HBV targeted ribonuclease fusion protein prokaryotic expression vector and express it in E.coli. METHODS: The cDNAs encoding HBV targeted ribonuclease, human eosinophil-derived neurotoxin and HBV core protein were respectively cloned into prokaryotic expression vector pTAT-HA. Recombinant plasmids were transformed into E.coli BL21(DE3) LysS, then the transformed cells were induced with IPTG. The expression of the fusion proteins were analyzed by SDS-PAGE and Western blot. RESULTS: The three recombinant plasmids were constructed and expressed after IPTG induction successfully. CONCLUSION: The obtained Tat-HBV targeted ribonuclease fusion protein has laid the foundation for using TR in therapy of HBV infection.