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  • Blackwell Publishing Ltd  (4)
  • American Society of Hematology  (2)
  • 1995-1999  (6)
  • 1990-1994
  • 1980-1984
  • 1970-1974
  • 1930-1934
  • 1998  (6)
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Plant breeding 117 (1998), S. 0 
    ISSN: 1439-0523
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: The Russian wheat aphid (RWA), Diuraphis noxia (Mordvilko), has become a serious, perennial pest of wheat (Triticum aestivum L.) in many areas of the world. This study was initiated to determine the inheritance of RWA resistance in PI 140207 (a RWA-resistant spring wheat) and to determine its allelic relationship with a previously reported RWA resistance gene. Crosses were made between PI 140207 and ‘Pavon’ (a RWA-susceptible spring wheat). Genetic analysis was performed on the parents, F1, F2, backcross (BC) population and F2-derived F3 families. Analyses of segregation patterns of plants in the F1, F2, and BC populations, and F2-derived F3 families indicated single dominant gene control of RWA resistance in PI 140207. Results of the allelism test indicated that the resistance gene in PI 140207, while conferring distinctly different seedling reactions to RWA feeding, is the same as Dn 1, the resistance gene in PI 137739.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Marine mammal science 14 (1998), S. 0 
    ISSN: 1748-7692
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: The Rns protein of enterotoxigenic Escherichia coli (ETEC) and the VirF protein of Shigella flexneri are members of the AraC family of transcription regulators. Rns is required for positive activation of the CS1 fimbrial genes, while VirF is a positive regulator of an invasion gene regulon. The amino acid sequences of the proteins are 36% identical, and both proteins activate transcription in response to increases in temperature. Here, we show that Rns is capable of complementing fully a null mutation in the S. flexneri virF gene. However, the VirF protein cannot replace Rns as an activator of CS1 gene expression in ETEC. This failure is not due to the absence from ETEC of a co-factor required by VirF since it also occurs when the CS1 system is moved into an S. flexneri genetic background. Nor is it a function of growth medium composition or a failure in virF gene expression. Instead, these findings point to important differences in the mechanisms by which these related transcription factors regulate gene expression in Gram-negative pathogens.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 22 (1998), S. 0 
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The variable domains of a neutralising (prevents erythrocyte lysis) anti-pneumolysin monoclonal antibody have been cloned and expressed as functional protein in Escherichia coli. Purification of the anti-pneumolysin single-chain antibody fragment, via antibody-affinity or metal-chelate affinity chromatography, resulted in product that was predominantly in a dimeric or monomeric form, respectively. The dimeric single-chain antibody fragment showed a higher sensitivity and affinity for immobilised antigen in both ELISA and BIAcore studies. The dimeric single-chain antibody fragment was as effective at protecting erythrocytes from lysis as the parent monoclonal. The monomeric, low affinity single-chain antibody fragment, showed reduced neutralising potency. As antibiotic resistant Streptococcus pneumoniae strains continue to show an increasing word-wide distribution, recombinant, neutralising antibody fragments, may provide an additional class of molecules useful in the treatment of toxaemia.
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  • 5
    Publication Date: 1998-05-01
    Description: Intermittent painful crises due to vasoocclusion are the major clinical manifestation of sickle cell disease (SCD), but subclinical episodes may also occur. There is sparse evidence for the involvement of neutrophils in the pathophysiology of SCD, but production of cytokines by the damaged endothelium might influence neutrophil function and modulate responses to subsequent cytokine exposure. In addition, the activation of neutrophils in the microcirculation could itself exacerbate vasoocclusion. To test whether neutrophil inflammatory responses were altered in SCD, neutrophil phospholipase A2 and NADPH oxidase activity in response to in vitro priming by granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor-α (TNF-α) were measured both during and between painful crises. Resting levels of neutrophil phospholipase A2 activity in steady-state SCD (4.0% ± 0.5% of total cell radioactivity) were raised relative to control values (2.0% ± 0.2%, n = 10, P = .008). There was no defect of agonist-stimulated phospholipase A2 or NADPH oxidase activity in steady-state SCD; however, the ability of phospholipase A2 to respond to priming with GM-CSF was attenuated to 63% ± 17% of control values (n = 10,P = .04). Similarly, neutrophil NADPH oxidase activity after priming with GM-CSF and TNF-α was, respectively, 65% ± 11% (n = 7, P = .03) and 57% ± 7% of control (n = 10, P = .007) in steady-state disease, and was further reduced during painful vasoocclusive crises to 34% ± 9% and 25% ± 3% of control for GM-CSF and TNF-α, respectively. These data were not explained by poor splenic function or any racial factor, as normal cytokine responses were seen in splenectomized patients in remission from Hodgkin's disease and in healthy Afro-Caribbean subjects. Abnormal neutrophil cytokine priming responses were not observed in either patients with rheumatoid arthritis or iron-deficiency anemia. Our findings are indicative of an ongoing inflammatory state in SCD between painful crises involving neutrophil activation and an abnormality of cytokine-regulated neutrophil function, which may compromise the host defenses against certain microorganisms.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 6
    Publication Date: 1998-05-01
    Description: Intermittent painful crises due to vasoocclusion are the major clinical manifestation of sickle cell disease (SCD), but subclinical episodes may also occur. There is sparse evidence for the involvement of neutrophils in the pathophysiology of SCD, but production of cytokines by the damaged endothelium might influence neutrophil function and modulate responses to subsequent cytokine exposure. In addition, the activation of neutrophils in the microcirculation could itself exacerbate vasoocclusion. To test whether neutrophil inflammatory responses were altered in SCD, neutrophil phospholipase A2 and NADPH oxidase activity in response to in vitro priming by granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor-α (TNF-α) were measured both during and between painful crises. Resting levels of neutrophil phospholipase A2 activity in steady-state SCD (4.0% ± 0.5% of total cell radioactivity) were raised relative to control values (2.0% ± 0.2%, n = 10, P = .008). There was no defect of agonist-stimulated phospholipase A2 or NADPH oxidase activity in steady-state SCD; however, the ability of phospholipase A2 to respond to priming with GM-CSF was attenuated to 63% ± 17% of control values (n = 10,P = .04). Similarly, neutrophil NADPH oxidase activity after priming with GM-CSF and TNF-α was, respectively, 65% ± 11% (n = 7, P = .03) and 57% ± 7% of control (n = 10, P = .007) in steady-state disease, and was further reduced during painful vasoocclusive crises to 34% ± 9% and 25% ± 3% of control for GM-CSF and TNF-α, respectively. These data were not explained by poor splenic function or any racial factor, as normal cytokine responses were seen in splenectomized patients in remission from Hodgkin's disease and in healthy Afro-Caribbean subjects. Abnormal neutrophil cytokine priming responses were not observed in either patients with rheumatoid arthritis or iron-deficiency anemia. Our findings are indicative of an ongoing inflammatory state in SCD between painful crises involving neutrophil activation and an abnormality of cytokine-regulated neutrophil function, which may compromise the host defenses against certain microorganisms.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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