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  • Articles: DFG German National Licenses  (2)
  • 1995-1999  (2)
  • Bcl–2  (1)
  • Endothelin  (1)
  • FT synthesis
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  • Articles: DFG German National Licenses  (2)
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Year
Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Pulmonary hypertension in systemic lupus erythematosus (1999)
    Springer
    Rheumatology international 18 (1999), S. 147-151 
    Details
    ISSN: 1437-160X
    Keywords: Key words Systemic lupus erythematosus ; Pulmonary hypertension ; Echocardiography ; Cardiac catheterization ; Endothelin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A prospective echocardiographic and clinical study was performed on 84 Chinese patients with systemic lupus erythematosus (SLE) and 99 controls to investigate the prevalence and the mechanism of pulmonary hypertension (PH) in SLE. Comparison between Doppler estimation and catheterization measurement was made in 12 cases to validate the predictive method. Compared to normal subjects, lupus patients had significantly increased sys-tolic pulmonary artery pressure (SPAP) (29.59±12.52 vs 19.64±5.82, P〈0.001), mean pulmonary artery pressure (MPAP) (15.11±7.36 vs 10.21±4.72, P〈0.001) and total pulmonary resistance (TPR) (315.85±190.65 vs 220.37± 55.92, P〈0.001). Nine of the 84 patients presented PH, defined as SPAP 〉30 mmHg and MPAP 〉20 mmHg. Pulmonary hypertensive patients had higher serum endothelin (ET) than non-pulmonary hypertensive patients, were more commonly in active stages, and presented Raynaud's phenomenon and rheumatoid factors. ET level was correlated with echocardiographic pulmonary pressure. Pulmonary hypertension commonly occurs in Chinese patients with SLE (11%), and it correlates with the lupus activity and the elevation of serum endothelin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002960050074
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Overexpression of basic fibroblast growth factor (FGF–2) downregulates Bcl–2 and promotes apoptosis in MCF–7 human breast cancer cells (1999)
    Springer
    Breast cancer research and treatment 56 (1999), S. 151-165 
    Details
    ISSN: 1573-7217
    Keywords: apoptosis ; basic FGF ; Bax ; Bcl–2 ; breast cancer ; MCF–7 cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Basic fibroblast growth factor (bFGF, FGF–2), a classical transforming factor, mitogen, and survival factor in multiple cell types, and has a paradoxic role in mammary epithelial cell transformation and proliferation. We have also demonstrated that recombinant FGF–2 uncharacteristically promotes cell death in MCF–7 human breast cancer cells. In this study, we investigated the effects of FGF–2 overexpression on survival in the same MCF–7 cells. In eight breast cancer cell lines and two nontransformed mammary epithelial cell lines, we demonstrated that high levels of Bcl–2 are only expressed in cells with undetectable levels of FGF–2 on western blot. In retrovirally transduced MCF–7 cells expressing both cytoplasm– and nucleus–localizing FGF–2 species and ones expressing only cytoplasm–localizing FGF–2 species, Bcl–2 levels were strongly decreased at both the mRNA and protein levels. Immunoprecipitation of Bax demonstrated a decreased association of Bax with Bcl–2 in these cells. Levels of Bax did not correlate with expression of FGF–2 in the 10 cell lines or in MCF–7 cells. The clonogenic potential of MCF–7 cells in tissue culture was decreased by the expression of FGF–2 and was additively suppressed by the chemotherapeutic agents etoposide and 5–fluorouracil in a dose and time dependent manner. MCF–7 cells overexpressing FGF–2 had a greater rate of programmed cell death at baseline and in response to etoposide and 5–fluorouracil in a TUNEL assay by immunofluorescent microphotography and by flow cytometric quantitation. The pro–apoptotic effect of FGF–2 overexpression on the chemosensitivity of these cells was confirmed by quantitative morphologic determination. These data demonstrate that the expression of FGF–2 downregulates Bcl–2 and promotes programmed cell death in MCF–7 human breast cancer cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006258510381
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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