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  • 1
    Electronic Resource
    Electronic Resource
    Early prediction of chronic lung disease by tracheal aspirate cytology in ventilated newborns (1999)
    Springer
    European journal of pediatrics 158 (1999), S. 234-237 
    Details
    ISSN: 1432-1076
    Keywords: Key words Squamous metaplasia ; Chronic lung disease ; Tracheal aspirate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We assessed the specificity of squamous metaplasia in tracheal aspirates of 69 ventilated newborns (gestational age 25–41 weeks) between days 3 and 7 of life for prediction of chronic lung disease (CLD). CLD was diagnosed when the patient was still requiring ventilation or supplementary oxygen at the postconceptional age of 36 weeks (or postnatal age of 28 days for babies born after 32 weeks gestation) and showed X-ray changes compatible with CLD. In the total population the presence of squamous metaplasia had a sensitivity of 59% and a specificity of 74% for the early diagnosis of CLD. The combination of squamous metaplasia and very low birth weight (VLBW) had a much higher specificity (94%), but a lower sensitivity (45%). Our results show that the presence of sqaumous metaplasia in VLBW babies during the 1st week of life predicts development of CLD with a specificity of 94% and may be helpful for entering patients into early treatment protocols or trials when a high risk population needs to be identified. As sensitivity of this approach is only 45%, further studies are needed to evaluate the predictive value of the combination of cytology with other markers in tracheal aspirate specimens. Conclusion The presence of squamous metaplasia in tracheal aspirates of VLBW babies between days 3 and 7 of life is significantly associated with the development of chronic lung disease. Simple microscopic evaluation of fresh tracheal aspirates enables us to identify patients at high risk of CLD at a very early stage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004310051057
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  • 2
    Electronic Resource
    Electronic Resource
    Activity of iodine-123 metaiodobenzylguanidine in childhood neuroblastoma: lack of relation to tumour differentiation in vivo (1998)
    Springer
    European journal of nuclear medicine 25 (1998), S. 144-149 
    Details
    ISSN: 1619-7089
    Keywords: Key words: Neuroblastoma ; Tumour differentiation ; Iodine-123 ; Metaiodobenzylguanidine ; Radionuclide imaging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Neuroblastoma (NB) tumour cells have a remarkable tendency to differentiate spontaneously or under the influence of certain drugs. It is not clear whether metaiodobenzylguanidine (MIBG) uptake correlates with differentiation of NB cells. In 28 tumours of 26 patients, iodine-123 MIBG uptake in primary NBs was studied in relation to tumour differentiation, tumour size, cell density and degree of necrosis in subsequently resected specimens. Genetic features such as the presence of chromosomal aberrations (1p-deletion and MYCN amplification) and/or P-glycoprotein (mdr-1 gene product) were also evaluated in relation to MIBG uptake. A highly variable and unpredictable intensity of MIBG uptake was observed in primary as well as secondary resected tumours. This intensity did not relate to any of the above-mentioned factors except that there was a trend towards more intense uptake with increasing size of the tumour. We conclude from our observations that, in contrast to commonly held opinion, well-differentiated tumours do not a priori show a lower MIBG uptake in vivo, even when there are a low number of viable cells and a high degree of necrosis. The degree of differentiation or tumour viability and necrosis following longstanding chemotherapeutic treatment cannot be predicted by the MIBG scan findings. The observed MIBG uptake may be importantly influenced by factors other than those associated with cellular differentiation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002590050207
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    Paper (German National Licenses)
    Fulltext
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