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Articles by Yue Huang
Total Records ( 3 ) for Yue Huang
  Wei Shi , Yue Huang , Mark Sutton-Smith , Berangere Tissot , Maria Panico , Howard R. Morris , Anne Dell , Stuart M. Haslam , Jeffrey Boyington , Barney S. Graham , Zhi- Yong Yang and Gary J. Nabel
  The Ebola virus nucleoprotein (NP) is an essential component of the nucleocapsid, required for filovirus particle formation and replication. Together with virion protein 35 (VP35) and VP24, this gene product gives rise to the filamentous nucleocapsid within transfected cells. Ebola virus NP migrates aberrantly, with an apparent molecular mass of 115 kDa, although it is predicted to encode an ~85-kDa protein. In this report, we show that two domains of this protein determine this aberrant migration and that this region mediates its incorporation into virions. These regions, amino acids 439 to 492 and amino acids 589 to 739, alter the mobility of Ebola virus NP by sodium dodecyl sulfate-polyacrylamide gel electrophoresis by 5 and 15 kDa, respectively, and confer similar effects on a heterologous protein, LacZ, in a position-independent fashion. Furthermore, when coexpressed with VP40, VP35, and VP24, this region mediated incorporation of NP into released viruslike particles. When fused to chimeric paramyxovirus NPs derived from measles or respiratory syncytial virus, this domain directed these proteins into the viruslike particle. The COOH-terminal NP domain comprises a conserved highly acidic region of NP with predicted disorder, distinguishing Ebola virus NPs from paramyxovirus NPs. The acidic character of this domain is likely responsible for its aberrant biochemical properties. These findings demonstrate that this region is essential for the assembly of the filamentous nucleocapsids that give rise to filoviruses.
  Yue Huang , Dejan Nikolic , Susan Pendland , Brian J. Doyle , Tracie D Locklear and Gail B. Mahady
  Cranberry, the fresh or dried ripe fruit of Vaccinium macrocarpon Ait. (Ericaceae), is currently used as adjunct therapy for the prevention and symptomatic treatment of urinary tract infections. Data from clinical trials suggest that extracts of cranberry or cranberry juice reduce the bacterial load of E. coli and also suppress the inflammatory symptoms induced by E. coli infections. A methanol extract prepared from 10 kg of dehydrated cranberries did not directly inhibit the growth of E coli strains ATCC 700336 or ATCC 25922 in concentrations up to 256 μg/mL in vitro. However, the methanol extract (CR-ME) inhibited the activity of cyclooxygenase-2, with an IC50 of 12.8 μg/mL. Moreover, CR-ME also inhibited the NF-κβ transcriptional activation in human T lymphocytes with an IC50 of 19.4 μg/mL, and significantly (p < 0.01) inhibited the release of interleukin (IL)-1β, IL-6, IL-8 and tumor necrosis factor-α from E. coli lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells in vitro, at a concentration of 50 μg/mL. The extract had no effect on inducible nitric oxide synthase activity in the murine macrophage cell line RAW 264.7. The compounds responsible for this activity were identified using a novel LC-MS based assay as ursolic acid and ursolic acid derivatives. Taken together, these data suggest CR-ME and its constituent chemical compounds target specific pathways involved in E. coli-induced inflammation.
  Kristen Gaus , Yue Huang , Dawn A. Israel , Susan L. Pendland , Bolanle A. Adeniyi and Gail B. Mahady
  Previous investigations demonstrated that a standardized extract of ginger rhizome inhibited the growth of Helicobacter pylori in vitro with a minimum inhibitory concentration in the range 0.78 to 12.5 μg/mL. In the present work, the extract was tested in a rodent model of H. pylori-induced disease, the Mongolian gerbil, to examine the effects of the extract on both prevention and eradication of infection. The extract was administered to Mongolian gerbils at a daily dose of 100 mg/kg body weight in rations either 3 weeks prior to infection or 6 weeks post-infection. Treatment with the standardized ginger extract reduced H. pylori load as compared with controls and significantly (P<0.05) reduced both acute and chronic muscosal and submucosal inflammation, cryptitis, as well as epithelial cell degeneration and erosion induced by H. pylori. Importantly, the extract did not increase morbidity or mortality. Further investigations of the mechanism demonstrated that the ginger extract inhibited the activity of cyclooxygenase-2, with 50% inhibitory concentration (IC50) of 8.5 μg/mL in vitro, inhibited the nuclear factor-κβ transcriptional response in kBZ Jurkat cells (human T lymphocytes) with an IC50 of 24.6 μg/mL, and significantly inhibited the release of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α from lipopolysaccharide-stimulated human peripheral blood mononuclear cells with IC50 values of 3.89, 7.7, 8.5, and 8.37 μg/mL, respectively. These results suggest ginger extracts may be useful for development as agents to reduce H. pylori-induced inflammation and as for gastric cancer chemoprevention.
 
 
 
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