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  • 1
    ISSN: 1437-9813
    Keywords: Key words Congenital diaphragmatic hernia ; Lung hypoplasia ; Nitrofen ; Thyroid transcription factor 1 ; Hepatocyte nuclear factor 3
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prenatal exposure to nitrofen induces lung hypoplasia and diaphragmatic hernias very similar to those in human disease, but the mechanisms are still unknown. Thyroid transcription factor 1 (TTF-1) is involved in lung ontogeny and regulation of the expression of surfactant proteins, and is likely abnormally expressed in nitrofen-induced lung hypoplasia. This study examines the effect of nitrofen on TTF-1 messenger RNA (mRNA) expression in the lungs of prenatal rat fetuses and a human lung-cell line (NCI-H441) that expresses both TTF-1 and surfactant proteins in vivo. Lungs from preterm fetuses harvested from rats with 100 mg nitrofen on gestational day 9.5 and NCI-H441 cells maintained in RPMI medium containing 10% fetal bovine serum and exposed to nitrofen for different times and concentrations were assayed for TTF-1 mRNA by northern blot analysis. mRNA for TTF-1 was decreased in nitrofen-exposed pups in comparison with controls, and exposure to nitrofen caused a dose- and time-related decrease in TTF-1 expression in H441 cell cultures. These results indicate that nitrofen downregulates TTF-1 both in vivo and in vitro. Since this interferes with lung development, it is reasonable to accept that lung hypoplasia in this model is in part due to the direct effect of the teratogen rather than to compression by the abdominal viscera herniated into the thorax. This mechanism should be explored in the clinical setting.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2568
    Keywords: Helicobacter pylori ; eradication therapy ; cell proliferation ; gastric cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Helicobacter pylori infection has been linked with gastric carcinoma. Epithelial cell proliferation is an indicator of cancer risk. The aim of this study was to assess gastric epithelial cell proliferation before and after eradication therapy and to assess the efficacy of treatment ofH. pylori infection using lanzoprazole and clarithromycin. Twenty-three patients withH. pylori-associated gastritis were treated with lanzoprazole 30 mg daily for four weeks and clarithromycin 500 mg three times a day for two weeks. Antral mucosal biopsies were taken for gastric epithelial cell proliferation analysis using thein vitro bromodeoxyuridine (BrdU) immunohistochemical technique before and four weeks after eradication therapy. Labeling index percent (LI%) was calculated as the percent ratio of proliferating cells to the total number of cells in the gastric pit. Efficacy of treatment was assessed in 16 subjects. Eight were negative forH. pylori infection 28 days after therapy and in eight patientsH. pylori infection was not eradicated. The eradication rate for the regimen was 50%. Cell kinetics were assessed in 19 subjects who completed treatment. Patients withH. pylori infection had a significantly higher LI% compared to normal (N=19, LI%: 5.01±0.3 vs 3.2±0.2,N=29). Eradication ofH. pylori infection significantly reduced epithelial cell proliferation (N=9, LI%:5.2±0.4 to 3.2 ±0.8,P〈0.001), whereas it was unaltered in those whose infection was not eradicated (N=10, LI%: 4.8±0.4 to 5.5±0.5,P=0.18). Eradication ofH. pylori reduces gastric epithelial cell proliferation to normal levels and may reduce the long-term the risk of gastric carcinoma.
    Type of Medium: Electronic Resource
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