RÉSUMÉ
<p><b>OBJECTIVE</b>To study the expression of E-cadherin and beta-catenin in neuroblastomas of various degrees of differentiation, and to investigate their molecular mechanisms in correlation with clinicopathologic parameters.</p><p><b>METHODS</b>Immunohistochemistry EnVision method was used to detect E-cadherin and beta-catenin expression in 90 paraffin-embedded tissue samples of neuroblastomas. The methylation status of CpG islands of E-cadherin promoter was investigated by MSP in 7 fresh tissue and 24 paraffin-embedded tissue samples. The mutation status of exon 3 of beta-catenin gene was studied by PCR in 7 fresh tissue samples. Statistical analysis of the data was performed by SPSS software.</p><p><b>RESULTS</b>E-cadherin and beta-catenin were abnormally expressed in neuroblastomas in general. The expression of beta-catenin in well-differentiated neuroblastoms was markedly higher (47/70, 67.1%) than that of the poorly differentiated tumors (8/20, 40.0%). There was a markedly decreased expression of both genes in tumors with lymph node metastasis than those without. Demethylation was seen in some regions of the promoter of E-cadherin in 31 cases of nuroblatomas. PCR of the exon 3 of beta-catenin followed by DNA sequencing demonstrated rearrangements and mutations in 7 cases, including 2 cases harboring identical point mutation at gene position 27184, leading to a T-->A alteration.</p><p><b>CONCLUSIONS</b>The abnormal over-expression of E-cadherin in neuroblastomas is independent of the methylation status of their promoter sequences. The abnormal expression of beta-catenin may be related to mutational changes at exon 3 of the gene.</p>
Sujet(s)
Enfant , Enfant d'âge préscolaire , Femelle , Humains , Nourrisson , Mâle , Cadhérines , Génétique , Métabolisme , Ilots CpG , Génétique , Méthylation de l'ADN , ADN tumoral , Génétique , Exons , Ganglioneuroblastome , Génétique , Métabolisme , Anatomopathologie , Réarrangement des gènes , Métastase lymphatique , Tumeurs du médiastin , Génétique , Métabolisme , Anatomopathologie , Neuroblastome , Génétique , Métabolisme , Anatomopathologie , Mutation ponctuelle , Régions promotrices (génétique) , Génétique , Tumeurs du rétropéritoine , Génétique , Métabolisme , Anatomopathologie , Analyse de séquence d'ADN , bêta-Caténine , Génétique , MétabolismeRÉSUMÉ
Objective To investigate the acute toxicity, subacute toxicity, nasal membrane local toxicity of the Magnolia biondii Pamp volatile oil nanometer bangosome. Methods Kunming mice and SD rats were selected as experimental material. Kunming mice were used in the acute and subacute toxicity tests by intragastric administration of Magnolia biondii Pamp volatile oil nanometer bangosome with different dosage and different time, and SD rats were used in the nasal membrane local toxicity test by nose dropping, while the control group was treated with intragastric administration of or nose dropping with normal saline for the same dosage. The treatment course lasted fifteen days. At the end of the tests, the general condition, routine blood test, function index of live and kidney, organ humid weight index, histological changes of liver and kidney and ultra microstructure change of rat nasal membrane were obtained and compared with the control group. Results In the acute toxicity test, the daily maximum tolerant dosage by intragastric administration was equal to 222.7 times of the clinical routine, with no marked toxic reaction. In the subacute toxicity test, the general condition, blood test, organ humid weight index and histological changes of live and kidney in different dosage groups were similar to the control group. While in the function index of live and kidney, uric acid was stepped down in the middle and large dose groups, and total bilirubin was decreased in the large dose group. The nasal membrane local toxicity test revealed that there was little change in the ultra microstructure of rat nasal membrane.Conclusion The Magnolia biondii Pamp volatile oil nanometer bangosome may have little toxicity by intragastric administration and nose dropping.
RÉSUMÉ
Objective To investigate the toxicity of nasal membreane and ciliary of the Magnolia biondii Pamp volotile oil nanometer bangosome.Methods Toad palate and rat nasal membrane were used as experimental material,physiological saline and hydrochloride ephedrine as negative control.The Magnolia biondii Pamp volotile oil nanometer bangosome on ciliary movement were carried out using in vitro and electron microscope technique.Results The Magnolia biondii Pamp volotile oil nanometer bangosome had little cilitoxicity to toad palate and rat nasal membrane.Conc(?)sion The Magnolia biondii Pamp volotile oil nanometer bangosome had little cilitoxicity to membrane.
RÉSUMÉ
Objective To investigate the expression of immunohistochemistry of gastrin(GAS),somatostatin(SS),proliferating cell nuclear antigen(PCNA) and Fas-ligand(Fas-L) in the sinus ventriculi of children with pediatric gastritis and to explore the significance of their expression in the pathogenesis of pediatric chronic gastritis.Methods Fifty cases of the sinus ventriculi mucosa samples were enrolled in 3 groups:chronic gastritis,helicobacter pylori(Hp) positive(group A,n=20);chronic gastritis,Hp negative(group B,n=19);control group,normal sinus ventriculi mucosa,Hp negative(group C,n=11).Immunohistochemistry En Vision were carried out including GAS,SS,PCNA and Fas-L.Results In the expression of GAS and SS,the values of group A and B were comparatively higher than those of group C,but there was no significant difference among them in statistics.In the expression of PCNA,the value of group A was comparatively higher and that of group B.The value difference between 2 groups was significant(P=0.019);in the expression of Fas-L,no significant difference was found among these 3 groups.Conclusions Expressions of GAS and SS both increase in children with chronic gastritis and maybe the increase of GAS and SS play a role in the pathogenesis of pediatric chronic gastritis;Hp infection promotes the multiplication of the sinus ventriculi membrana mucosa epithelium cell in pediatric chronic gastritis.