Teresa Cepeda

Instituto de Salud Carlos III, Madrid, Madrid, Spain

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Publications (2)3.6 Total impact

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    ABSTRACT: The effect of in vivo chronic administration of recombinant human growth hormone (rhGH) on morphology and individual GH release in somatotroph cells was evaluated in young male Wistar rats. Over an 18-day period, 30-day-old male rats were injected daily with 1.5 1U rhGH/kg (GPG group) or saline (VPG group) by subcutaneous injection. Electron-immunocytochemical, ultrastructural and morphometric studies of somatotroph cells were carried out. Additionally, rat pituitary cells were dispersed and overall and individual GH release was studied by radioimmunoassay and cell immunoblot assay (quantified by image analysis), respectively. The ultrastructure and size of somatotroph cells did not change, but volume density of secretion granules was reduced (p<0.01) by previous in vivo GH treatment. At four days, basal GH release of rat pituitary cell monolayer cultures was lower in the GPG group than in the VPG group (p<0.05); after 12 hours of culture, GHRH stimulation of GH release was lower in the GPG group than in the VPG group (p<0.05), and GHRH+SRIH inhibited GH release in the GPG group (p<0.05), but not in the VPG group. The percentage of somatotroph cells was not modified, but the ratio of strongly/weakly GH-immunostained cells had changed; weakly GH-immunostained cells increased from 34% to 55%. Moreover, in vitro treatment with GHRH, SRIH, and both, easily changed the strongly/weakly GH-immunostained cell ratio. Individual GH release, however, was not changed by previous in vivo GH treatment, although GHRH preferably stimulated a subpopulation of GH cells and SRIH did not inhibit individual GH release. These data suggest that exogenous chronic rhGH treatment down-regulates somatotroph function by modifying the proportion of GH cell subpopulation.
    Histology and histopathology 04/2000; 15(2):375-83. · 2.24 Impact Factor
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    ABSTRACT: The nucleotide sequence of a 1620-bp chromosomal fragment from Streptococcus pneumoniae, containing a putative class-II aldolase gene, has been determined. The N-terminal amino acid (aa) sequence of S. pneumoniae class-II aldolase protein allowed us to determine the initiation site for the putative aldolase gene, and a molecular weight of 31,274 Da was predicted for the protein, after removal of the N-terminal methionine. Northern hybridization and primer extension analysis showed a 1100-nucleotide transcript with a transcription start site located 43 or 42 bp upstream of the start codon. Southern hybridization studies indicated that the putative class-II aldolase gene was in the ApaI fragment 6, SmaI fragment 9, and SacII fragment 12 or 13 of the physical map of S. pneumoniae chromosome. Southern hybridization analysis and partial sequencing performed in another eight streptococcus species, belonging to six different phylogenetic groups, suggested that a class-II aldolase gene with a considerable DNA homology to that of the S. pneumoniae, could exist in these streptococcal species.
    Current Microbiology 08/1999; 39(1):31-6. DOI:10.1007/PL00006823 · 1.36 Impact Factor