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  • 2000-2004  (3)
  • cystic fibrosis  (2)
  • Key words Apoptosis – myocardium – stunning – endothelin-1 – nitric oxide – ischemia – reperfusion  (1)
  • Analytical Chemistry and Spectroscopy
  • Inorganic Chemistry
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Year
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Glycoconjugate journal 17 (2000), S. 617-626 
    ISSN: 1573-4986
    Keywords: α1,3fucose ; α1,6fucose ; sialic acid ; polyα2,8sialic acid ; surface membrane glycoforms ; cystic fibrosis ; lactosylated polylysine gene therapy vector
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Terminal glycosylation has been a recurring theme of the laboratory. In cystic fibrosis (CF), decreased sialic acid and increased fucosyl residues in α1,3 position to antennary N -acetyl glucosamine is the CF glycosylation phenotype. The glycosylation phenotype is reversed by transfection of CF airway cells with wtCFTR. In neuronal cells, polymers of α2,8sialyl residues are prominent in oligodendrocytes and human neuroblastoma. These findings are discussed in relationship to early studies in our laboratories and those of other investigators. The potential extension of these concepts to future clinical therapeutics is presented.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-4986
    Keywords: glycosylation ; cystic fibrosis ; airway epithelial cells ; α1,3fucose ; sialic acid ; CFTR ; CFTR transfection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Cystic fibrosis (CF) has a characteristic glycosylation phenotype usually expressed as a decreased ratio of sialic acid to fucose. The glycosylation phenotype was found in CF/T1 airway epithelial cells (ΔF508/ΔF508). When these cells were transfected and were expressing high amounts of wtCFTR, as detected by Western blot analysis and in situ hybridization, the cell membrane glycoconjugates had an increased sialic acid content and decreased fucosyl residues in α1,3/4 linkage to antennary N[emsp4 ]-acetyl glucosamine (Fucα1,3/4GlcNAc). After the expression of wtCFTR decreased, the amount of sialic acid and Fucα1,3/4GlcNAc returned to levels shown by the parent CF cells. Sialic acid was measured by chemical analysis and Fucα1,3/4GlcNAc was detected with a specific α1,3/4 fucosidase. CF and non-CF airway cells in primary culture also had a similar reciprocal relationship between fucosylation and sialylation. It is possible that the glycosylation phenotype is involved in the pathogenesis of CF lung disease by facilitating bacterial colonization and leukocyte recruitment.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-1803
    Keywords: Key words Apoptosis – myocardium – stunning – endothelin-1 – nitric oxide – ischemia – reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective. Reperfusion injury may affect the cardiac NO and endothelin production. We investigated whether 20 min of total ischemia followed by 40 min of reperfusion can induce apoptosis in a Langendorff model of retrogradely perfused rat hearts (37°C; paced at 300/’), and we attempted to correlate these findings with measured tissue NO and ET-1 levels. Methods. An apoptosis detection system was utilized which catalytically incorporates fluorescein-12-dUTP at the 3’-OH DNA ends using the principle of the TUNEL assay, with direct visualization of the labeled DNA. ET-1 was measured by radioimmunoassay and NO3/NO2 by ion pairing HPLC on C18 reverse phase columns. Results. None of the postischemic (n = 6) nor of the control perfused (90 min, n = 6) hearts showed signs of apoptosis, while those exposed to longer ischemia (40 min) and reperfusion (2 h) confirmed the presence of apoptotic cells. Myocardial ET-1 concentrations were 4.8±1.0 versus 8.3±2.5 pg/100 mg (control vs. ischemic hearts, respectively; mean ±SD; p 〈 0.05). Myocardial NO contents showed no differences. Conclusion. These data suggest that the time window of apoptosis with detectable DNA fragmentation exceeds 20 min of global total ischemia and 40 min of reperfusion, a model frequently used for inducing myocardial stunning. While NO was not increased in postischemic hearts, increased ET-1 levels indirectly argue for a role of ET-1 as inducer of apoptosis, but only at a later stage of reperfusion.
    Type of Medium: Electronic Resource
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